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17 pages, 2052 KiB  
Systematic Review
Effect of Resistance Training on Older Adults with Sarcopenic Obesity: A Comprehensive Systematic Review and Meta-Analysis of Blood Biomarkers, Functionality, and Body Composition
by Luis Polo-Ferrero, Víctor Navarro-López, Manuel Fuentes, Jesus Lacal, María Dolores Cancelas-Felgueras, Natalia Santos-Blázquez, Roberto Méndez-Sánchez and Juan Luis Sánchez-González
Nurs. Rep. 2025, 15(3), 89; https://doi.org/10.3390/nursrep15030089 - 4 Mar 2025
Abstract
Background/Objectives: Sarcopenic obesity (SO) is a clinical condition in which there is an excess of fat mass and a loss of muscle mass, strength, and function. Its prevalence increases with age, particularly in adults over 65 years old. However, debate persists on [...] Read more.
Background/Objectives: Sarcopenic obesity (SO) is a clinical condition in which there is an excess of fat mass and a loss of muscle mass, strength, and function. Its prevalence increases with age, particularly in adults over 65 years old. However, debate persists on the definition and assessment of SO. The purpose of this review is to examine the impact of resistance training on older adults with sarcopenic obesity. Methods: This review included studies investigating the effects of resistance training interventions in older adults with SO. A comprehensive literature search was conducted across six databases (PubMed, SCOPUS, Cochrane Library, Embase, EBSCO, and Web of Science), yielding 1882 articles. The risk of bias in the included studies was assessed using the PEDro scale and the GRADE system. Results: Eleven randomized clinical trials were analyzed qualitatively and nine were analyzed quantitatively. The meta-analysis demonstrated that exercise interventions revealed the positive effects of exercise mainly on physical performance ([SMD] = 0.36, [95% CI] = 0.03, 0.69, p = 0.003) and body composition ([SMD] = 0.35, [95% CI] = 0.12, 0.57, p = 0.003), with no significant differences in biomarkers ([SMD] = 0.1, [95% CI] = −0.28, 0.49, p = 0.52). Conclusions: Resistance training benefits older adults with SO, improving body composition and physical function, whereas there were no significant differences in blood biomarkers. The present review highlights the limitations of the existing evidence base. Many included studies exhibited methodological shortcomings, necessitating the cautious interpretation of findings. Future research should prioritize rigorous study designs, including larger sample sizes and extended follow-up periods, to enhance the precision and generalizability of results. Full article
(This article belongs to the Special Issue Nursing Interventions to Improve Healthcare for Older Adults)
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Figure 1
<p>PRISMA flow diagram [<a href="#B41-nursrep-15-00089" class="html-bibr">41</a>].</p>
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<p>Forest plot of the results of a random-effects meta-analysis for the comparison of body composition, shown as standardized mean differences (SMDs) with 95% CIs. Shaded squares represent point estimates for each individual study and the weight of the study in the meta-analysis. Diamonds represent the overall mean difference of the studies [<a href="#B49-nursrep-15-00089" class="html-bibr">49</a>,<a href="#B54-nursrep-15-00089" class="html-bibr">54</a>,<a href="#B55-nursrep-15-00089" class="html-bibr">55</a>,<a href="#B56-nursrep-15-00089" class="html-bibr">56</a>,<a href="#B57-nursrep-15-00089" class="html-bibr">57</a>,<a href="#B58-nursrep-15-00089" class="html-bibr">58</a>,<a href="#B59-nursrep-15-00089" class="html-bibr">59</a>].</p>
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<p>Forest plot of the results of a random-effects meta-analysis for the comparison of physical performance, shown as SMDs with 95% CIs. Shaded squares represent point estimates for each individual study and the weight of the study in the meta-analysis. Diamonds represent the overall mean difference of the studies [<a href="#B56-nursrep-15-00089" class="html-bibr">56</a>,<a href="#B57-nursrep-15-00089" class="html-bibr">57</a>,<a href="#B58-nursrep-15-00089" class="html-bibr">58</a>,<a href="#B59-nursrep-15-00089" class="html-bibr">59</a>].</p>
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<p>Forest plot of the results of a random-effects meta-analysis for the comparison of biomarkers, shown as SMDs with 95% CIs. Shaded squares represent point estimates for each individual study and the weight of the study in the meta-analysis. Diamonds represent the overall mean difference of the studies [<a href="#B52-nursrep-15-00089" class="html-bibr">52</a>,<a href="#B55-nursrep-15-00089" class="html-bibr">55</a>,<a href="#B56-nursrep-15-00089" class="html-bibr">56</a>].</p>
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20 pages, 1100 KiB  
Article
Sprinters’ and Marathon Runners’ Performances Are Better Explained by Muscle Fibers’ Percentage Cross-Sectional Area than Any Other Parameter of Muscle Fiber Composition
by Spyridon Methenitis, Angeliki-Nikoletta Stasinaki, Thomas Mpampoulis, Constantinos Papadopoulos, Giorgos Papadimas, Nikolaos Zaras and Gerasimos Terzis
Sports 2025, 13(3), 74; https://doi.org/10.3390/sports13030074 - 4 Mar 2025
Viewed by 22
Abstract
The present study aimed to investigate the correlation between muscle fiber type variables and sprinting, jumping, strength, power and endurance performances in sprinters and marathon runners. Furthermore, the study explored which muscle fiber type variable influences athletes’ performance the most and which variable [...] Read more.
The present study aimed to investigate the correlation between muscle fiber type variables and sprinting, jumping, strength, power and endurance performances in sprinters and marathon runners. Furthermore, the study explored which muscle fiber type variable influences athletes’ performance the most and which variable discriminates sprinters from marathon runners. Body composition, vastus lateralis muscle fiber composition, sprinting, jumping, strength, maximum isometric force, rate of force development and endurance performance were assessed in well-trained sprinters (n = 15; age: 24.7 ± 4.1 years; body mass: 82.7 ± 8.8 kg; body fat: 11.3 ± 4.2%) and marathon runners (n = 15; age: 26.1 ± 3.2 years; body mass: 69.7 ± 4.3 kg; body fat: 9.5 ± 3.3%). Significant correlations were observed between muscle fiber composition variables and performances (r = −0.848 to 0.902; p < 0.05), with percentage cross-sectional areas (%CSAs) showing the strongest associations. Regression analyses confirmed %CSAs as the strongest predictors of performance (R2: 0.796–0.978; p < 0.001; B coefficients: −0.293–0.985), while discriminant analysis accurately differentiated sprinters from marathon runners (100%, p < 0.001) by only using athletes’ muscle fibers’ %CSAs. In conclusion, muscle fibers’ %CSAs may be the most critical variables for explaining and distinguishing sprinters’ and marathon runners’ performances. Full article
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<p>Correlation plots between vastus lateralis percentage areas occupied by Type I, IIa muscle fibers, estimated maximum oxygen consumption (<b>A</b>,<b>B</b>) and maximum aerobic velocity (<b>C</b>,<b>D</b>) for all athletes as one group (n = 30) as well as separately for Sprinters (n = 15) and Marathon Runners (n = 15).</p>
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17 pages, 876 KiB  
Article
Adapting Overwintering Honey Bee (Apis mellifera L.) Colony Management in Response to Warmer Fall Temperatures Associated with Climate Change
by Gloria DeGrandi-Hoffman, Henry Graham, Vanessa Corby-Harris, Mona Chambers, Emily Watkins-deJong, Kate Ihle and Lanie Bilodeau
Insects 2025, 16(3), 266; https://doi.org/10.3390/insects16030266 - 4 Mar 2025
Viewed by 101
Abstract
Management strategies are needed that mitigate the effects of climate change on honey bee colony losses. Extended periods of warmer fall temperatures prolong periods of honey bee flight and parasitic Varroa mite immigration into colonies. We report on a management strategy using Varroa-resistant [...] Read more.
Management strategies are needed that mitigate the effects of climate change on honey bee colony losses. Extended periods of warmer fall temperatures prolong periods of honey bee flight and parasitic Varroa mite immigration into colonies. We report on a management strategy using Varroa-resistant Russian honey bees overwintered in indoor cold storage facilities, and compare colony survival and growth with that of unselected European bees. Fat body metrics that are key to overwintering survival were also measured in Russian and unselected bees. Comparisons between overwintering Russian colonies in cold storage versus apiaries were also conducted. Russian and unselected colonies overwintered in cold storage had comparable overwintering survival and percentages rented for almond pollination. However, more Russian colonies overwintered in cold storage were alive after almond bloom than those overwintered in apiaries. Fat bodies in Russian and unselected bees gained weight while in cold storage. Protein concentrations increased and lipids decreased. Changes in lipid concentrations were inversely related to the number of brood bees reared while in cold storage. Similar percentages of colonies overwintered in cold storage or outdoor apiaries survived and were rented for almond pollination. An economic analysis indicated that overwintering Russian colonies in cold storage costs less than in apiaries. Our study indicates that cold storage can be a viable management strategy for mitigating the effects of climate change on colony survival. Full article
(This article belongs to the Special Issue Bee Health and Beehive Management in a Changing World)
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<p>The locations of colonies used in this study. Colonies headed by unselected (UNSEL) European queens spent the summer in Baldwin, North Dakota, and those headed by Russian (RUS) queens spent the summer in Hebron, North Dakota. In October, RUS and UNSEL colonies were moved to cold storage facilities in Filer, Idaho, for overwintering. Concurrently, a group of RUS colonies were moved from Hebron, North Dakota, to outdoor apiaries in Wiggins, Mississippi, for overwintering (RUSms). In January, UNSEL, RUS, and RUSms colonies were moved to almond orchards in Madera County, California, for pollination.</p>
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<p>Average (with standard error bars) combs with bees (<b>a</b>) and brood (<b>b</b>) in colonies headed by either Russian (RUS) or unselected (UNSEL) European queen lines. Combs with bees were significantly affected by queen line (F<sub>1,474</sub> = 9.57, <span class="html-italic">p</span> = 0.002), sample time (F<sub>2,474</sub> = 111.4, <span class="html-italic">p</span> &lt; 0.0001), and interactions between the factors (F<sub>1,304</sub> = 7.19, <span class="html-italic">p</span> = 0.001). Combs of brood were affected by sample time (F<sub>1,304</sub> = 233.8, <span class="html-italic">p</span> &lt; 0.0001) but not queen line (F<sub>1,304</sub> = 0.94, <span class="html-italic">p</span> = 0.33) or interactions between the factors (F<sub>1,304</sub> = 0.82, <span class="html-italic">p</span> = 0.36). The average number of combs of sealed brood after cold storage was significantly higher in UNSEL than RUS (t<sub>143</sub> =2.86, <span class="html-italic">p</span> = 0.005) but not after almond bloom (t<sub>133</sub> = 1.65, <span class="html-italic">p</span> = 0.10). There were no differences between the percentage of RUS and UNSEL colonies that survived cold storage overwintering (<span class="html-italic">p</span> = 0.12), could be rented for almond pollination (<span class="html-italic">p</span> = 0.51), and were alive after almond bloom (<span class="html-italic">p</span> = 0.77) (<b>c</b>). Standard error bars are shown with the percentages. An asterisk (*) over a bar indicates significant differences at the <span class="html-italic">p</span> = 0.05 level between RUS and UNSEL as determined by Student’s <span class="html-italic">t</span>-tests.</p>
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<p>Average dry weight (<b>a</b>) and lipid (<b>b</b>) and protein (<b>c</b>) concentrations (with standard error bars) in fat bodies of worker bees from colonies of Russian and unselected European queen lines prior to (pre-cold storage) and after (post-cold storage) overwintering in cold storage. All measurements were made from pooled samples of 10 bees per colony. Fat body metrics were estimated using 30 colonies per queen line. Fat body weights did not differ between queen lines (F<sub>1,113</sub> = 1.5; <span class="html-italic">p</span> = 0.22) but did differ between sample times (F<sub>1,113</sub> = 29.0, <span class="html-italic">p</span> &lt; 0.0001). The interaction term (sample time × queen line) was significant (F<sub>1,113</sub> = 11.08, <span class="html-italic">p</span> = 0.001). Lipid concentrations differed by queen line (F<sub>1,113</sub> = 13.2, <span class="html-italic">p</span> &lt; 0.0001) and sample time (F<sub>1,113</sub> = 36.05, <span class="html-italic">p</span> &lt; 0.0001). Interactions terms were significant (F<sub>1,113</sub> = 19.06, <span class="html-italic">p</span> &lt; 0.0001). Protein concentrations differed by queen line (F<sub>1,113</sub> = 5.40, <span class="html-italic">p</span> = 0.022) and sample time (F<sub>1,113</sub> = 88.25, <span class="html-italic">p</span> &lt; 0.0001). Interaction terms were significant (F<sub>1,113</sub> = 8.66, <span class="html-italic">p</span> = 0.004). An asterisk (*) over a bar indicates significant differences at the <span class="html-italic">p</span> = 0.05 level between RUS and UNSEL as determined by Student’s <span class="html-italic">t</span>-tests.</p>
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20 pages, 1900 KiB  
Article
Criterion-Related Validity and Reliability of the Front Plank Test in Adults: The ADULT-FIT Project
by Ángela Rodríguez-Perea, Pedro Aragón-Aragón, Magdalena Cuenca-García, Carolina Cruz-León, Maximiliano Torres-Banduc, Sandra Sánchez-Parente and José Castro-Piñero
Appl. Sci. 2025, 15(5), 2722; https://doi.org/10.3390/app15052722 - 4 Mar 2025
Viewed by 141
Abstract
Background: the validity and reliability of the front plank test (FPT) have been studied in young adults but not in adults aged 34 to 60 years. The aim of this study was to analyze the criterion-related validity and reliability of the front plank [...] Read more.
Background: the validity and reliability of the front plank test (FPT) have been studied in young adults but not in adults aged 34 to 60 years. The aim of this study was to analyze the criterion-related validity and reliability of the front plank test (FPT) for evaluating trunk musculature in adults according to sex and age groups. Methods: a repeated measures design was used to study the reliability of the FPT. A total of 84 adults aged 18–62 years performed trunk muscular force tests and the FPT. Criterion-related validity was assessed using repeated measures ANOVA. Reliability was examined by ICC, error measurements, and Bland–Altman analysis across sex and age groups. Results: significant differences in the activation of the rectus abdominis and external oblique muscles were found compared with the erector spinae and multifidus muscles (p < 0.001). No correlations were found between FPT time and physical activity or rate of perceived exertion at the end (p > 0.05). Low and moderate correlations were found with body fat percentage, trunk fat mass percentage, and external oblique, regardless of sex and age groups (p < 0.05). Extremely high reliability was found regardless of sex and age groups (ICC > 0.98), with low error measurements (RMSE = 11.93–18.73; %CV = 4.91–6.33; SEE = 11.45–16.84). MDC90 values indicated no real change between T1 and T2. Conclusion: FPT is a valid and reliable test for assessing trunk musculature in adults regardless of sex and age groups. Full article
(This article belongs to the Special Issue Sports Biomechanics and Sports Technology)
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<p>Set up of the front plank test.</p>
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<p>Exercises performed for maximal voluntary isometric contraction of (<b>A</b>) upper and lower rectus abdominis, (<b>B</b>) external oblique, and (<b>C</b>) erector spinae and multifidus.</p>
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<p>Electromyographic activity of trunk muscles during the front plank test. Difference in the EMG data of the trunk muscles (URA, LRA, EO, MF, and ES). MVIC = maximum voluntary isometric contraction; RA = rectus abdominis. Significance level *** = statistically significant (<span class="html-italic">p</span> &lt; 0.001) for the erector spinae and multifidus muscles.</p>
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<p>The Bland–Altman plot depicts the averaged difference between test and retest of FPT and 95% limits of agreement (dashed lines), along with the regression line (solid line). In addition, a solid line indicates the 0 point. (<b>A</b>) Whole sample. (<b>B</b>) Male. (<b>C</b>) Female. (<b>D</b>) Young adults. (<b>E</b>) Adults.</p>
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25 pages, 33164 KiB  
Article
Poria cocos-Derived Exosome-like Nanovesicles Alleviate Metabolic Dysfunction-Associated Fatty Liver Disease by Promoting Mitophagy and Inhibiting NLRP3 Inflammasome Activation
by Tao Wang, Jun Zhao, Qiu-Yi Li, Hui-Qiong Yang, Min Li, Rong Duan, Mei Zhang, Yan Qi, Jie Yu and Xing-Xin Yang
Int. J. Mol. Sci. 2025, 26(5), 2253; https://doi.org/10.3390/ijms26052253 - 3 Mar 2025
Viewed by 114
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) affects approximately one-quarter of the world’s adult population, and no effective therapeutic drugs are available. Poria cocos is a fungus used as a herb and food nutrient for centuries as well as for MAFLD treatment. Exosome-like nanovesicles [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MAFLD) affects approximately one-quarter of the world’s adult population, and no effective therapeutic drugs are available. Poria cocos is a fungus used as a herb and food nutrient for centuries as well as for MAFLD treatment. Exosome-like nanovesicles have many pharmacological activities; however, studies on the effects of Poria cocos-derived exosome-like nanovesicles (PCELNs) on MAFLD are lacking. Therefore, our study aimed at identifying the effects and mechanism of action of PCELNs on MAFLD. PCELNs were isolated by ultracentrifugation and their morphology was characterized, such as particle size, zeta potential, protein distributions, as well as lipid and miRNA compositions. Then, the absorption and distribution of PCELNs were observed in vivo and in vitro. Finally, L02 cell steatosis model induced by fat emulsion and MAFLD mouse model induced by high-fat diet (HFD) were used to evaluate the effect and mechanism of PCELNs on MAFLD. PCELNs were membrane structured vesicles, with a particle size of 161.4 ± 1.7 nm, a zeta potential of −3.20 ± 0.37 mV, and contained a range of proteins, lipids, and miRNAs. PCELNs were absorbed by L02 cells and targeted the liver and spleen after intraperitoneal injection. PCELNs inhibited body weight gain and improved the index of heart, liver, spleen, and various fats, as well as decreased lipid accumulation and lipid level. They also protected mitochondrial ultrastructure and regulated oxidative stress and energy metabolism disorder. Furthermore, PCELNs increased PTEN induced kinase 1 (PINK1), E3 ubiquitin ligase (Parkin) and microtubule associated protein light chain-3 (LC3) protein expression in the liver, reduced oxidized mitochondrial DNA (Ox-mtDNA) content in mitochondria and cytoplasm of the liver, reduced nucleotide binding oligomerization domain-like receptor protein 3 (NLRP3), pro-cysteinyl aspartate specific proteinase-1 (caspase-1), cleared-caspase-1, and mature-interleukin-1β (IL-1β) protein expression in the liver, and reduced the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, and interleukin-18 (IL-18) in serum and liver. In conclusion, we demonstrated that PCELNs may alleviate HFD-induced MAFLD by promoting mitochondrial autophagy and inhibiting NLRP3 inflammasome activation. Full article
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Figure 1
<p>Physicochemical characterization and composition of PCELNs. (<b>A</b>) TEM image of PCELNs (scale bar = 100 nm). (<b>B</b>,<b>C</b>) Size distribution of PCELNs. (<b>D</b>) Zeta potential of PCELNs (Repeat the test three times). (<b>E</b>) Protein gel electrophoresis of PCELNs. (<b>F</b>) TLC image and (<b>G</b>) lipidomic analysis of PCELNs. (<b>H</b>) Classification of small nucleic acids contained in PCELNs. (<b>I</b>) Composition and proportion of top 10 miRNAs in PCELNs. (<b>J</b>) GO and (<b>K</b>) KEGG enrichment analysis of top 10 miRNAs in PCELNs. PCELNs, <span class="html-italic">Poria cocos</span>-derived exosome-like nanovesicles; TEM, transmission electron microscope; TLC, thin-layer chromatography; GO, Gene Ontology; KEGG, Kyoto encyclopedia of genes and genomes.</p>
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<p>Biocompatibility and cytotoxicity of PCELNs. (<b>A</b>) Uptake of PCELNs by L02 cells at different times and concentrations (scale bar = 10 µm). (<b>B</b>) Cytotoxicity of PCELNs on L02 cells for 24 h and 48 h. <span class="html-italic">n</span> = 3. Results were expressed as mean ± S.D.</p>
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<p>Effect of PCELNs on L02 cells. (<b>A</b>) Images of oil red O staining (scale bar = 100 µm). (<b>B</b>) Analysis of relative fat content. Cell levels of (<b>C</b>) TC, (<b>D</b>) TG, (<b>E</b>) ALT, (<b>F</b>) AST, (<b>G</b>) GSH, (<b>H</b>) SOD, (<b>I</b>,<b>J</b>) ROS, (<b>K</b>) Na<sup>+</sup>-K<sup>+</sup>-ATPase, (<b>L</b>) Ca<sup>2+</sup>-Mg<sup>2+</sup>-ATPase, (<b>M</b>) complex I, and (<b>N</b>) complex II. <span class="html-italic">n</span> = 3. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. NC, normal control; MOD, high-fat diet; FC, fenofibrate capsules; TG, triglyceride; TC, total cholesterol; AST, aspartate transaminase; ALT, alanine transaminase; SOD, superoxide dismutase; GSH, glutathione; ROS, reactive oxygen species; ATPase, ATP synthase; complex I, respiratory chain complex I; complex II, respiratory chain complex II.</p>
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<p>Effect of PCELNs on PINK1/Parkin-mediated mitophagy in L02 cells. (<b>A</b>) immunofluorescence images of PINK1, Parkin, LC3, and p62 (scale bar = 50 µm). Analysis of relative fluorescence intensity of (<b>B</b>) PINK1, (<b>C</b>) Parkin, (<b>D</b>) p62, and (<b>E</b>) LC3. <span class="html-italic">n</span> = 3. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. PINK1, PTEN induced kinase 1; Parkin, E3 ubiquitin ligase; LC3, microtubule associated protein light chain-3; p62, sequestosome 1.</p>
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<p>Biodistribution of PCELNs. (<b>A</b>) Biodistribution of PCELNs in mice after intraperitoneal injection. (<b>B</b>) Biodistribution of PCELNs in organs after intraperitoneal injection.</p>
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<p>Effect of PCELNs on body weight, food intake, organs, and fat index. (<b>A</b>) Body weight. (<b>B</b>) Body weight in last week. (<b>C</b>) Average daily food intake. (<b>D</b>) Heart, (<b>E</b>) liver, (<b>F</b>) spleen, (<b>G</b>) lung, (<b>H</b>) kidney, (<b>I</b>) WATi, (<b>J</b>) WATg, and (<b>K</b>) BAT index. <span class="html-italic">n</span> = 6. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. WATg, gonad white adipose tissue; WATi, inguinal white adipose tissue; BAT, brown adipose tissue; NC, normal control; MOD, high-fat diet; FC, fenofibrate capsules; LPCELNs, low PCELN-treated group; MPCELNs, middle PCELN-treated group; HPCELNs, high PCELN-treated group.</p>
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<p>Effect of PCELNs on serum lipid-related parameters. Serum levels of (<b>A</b>) TC, (<b>B</b>) TG, (<b>C</b>) ALT, (<b>D</b>) AST, (<b>E</b>) HDL-C, (<b>F</b>) LDL-C. <span class="html-italic">n</span> = 6. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol.</p>
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<p>Effect of PCELNs on liver lipid metabolism. (<b>A</b>) Images of oil red O staining (scale bar = 50 µm). (<b>B</b>) Analysis of relative fat content. (<b>C</b>) Hematoxylin and eosin (H&amp;E) images. Liver levels of (<b>D</b>) TC, (<b>E</b>) TG, (<b>F</b>) ALT, (<b>G</b>) AST, (<b>H</b>) LDL-C, and (<b>I</b>) HDL-C. <span class="html-italic">n</span> = 6. Results were expressed as mean ± S.D. ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group.</p>
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<p>Effect of PCELNs on serum and liver inflammatory factors. Serum levels of (<b>A</b>) TNF-α, (<b>B</b>) IL-6, (<b>C</b>) IL-1β, and (<b>D</b>) IL-18. Expression of (<b>E</b>) TNF-α, (<b>F</b>) IL-6, (<b>G</b>) IL-1β, and (<b>H</b>) IL-18 in liver. <span class="html-italic">n</span> = 6. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. TNF-α, tumor necrosis factor-α; IL-6, interleukin-6; IL-1β, interleukin-1β; IL-18, interleukin-18.</p>
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<p>Effect of PCELNs on mitochondrial ultrastructure and function in liver. (<b>A</b>) TEM image of mitochondria (scale bar = 5 µm). Levels of (<b>B</b>) MDA, (<b>C</b>) GSH, (<b>D</b>) SOD, (<b>E</b>) ROS, (<b>F</b>) Na<sup>+</sup>-K<sup>+</sup>-ATPase, (<b>G</b>) Ca<sup>2+</sup>-Mg<sup>2+</sup>-ATPase, (<b>H</b>) complex I, and (<b>I</b>) complex II. <span class="html-italic">n</span> = 6. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. MDA, malondialdehyde.</p>
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<p>Mitophagy was involved in inhibition of NLRP3 inflammasome by PCELNs. (<b>A</b>) Immunoblotting images of PINK1, Parkin, p62, and LC3. Relative expression of (<b>B</b>) PINK1, (<b>C</b>) Parkin, (<b>D</b>) p62, and (<b>E</b>) LC3. Levels of (<b>F</b>) mitochondrial Ox-mtDNA and (<b>G</b>) cytoplasmic Ox-mtDNA. (<b>H</b>) immunoblotting images of NLRP3, pro-caspase-1, cleared-caspase-1, and mature-IL-1β. Relative expression of (<b>I</b>) NLRP3, (<b>J</b>) pro-caspase-1, (<b>K</b>) cleared-caspase-1, and (<b>L</b>) mature-IL-1β. <span class="html-italic">n</span> = 3. Results were expressed as mean ± S.D. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. MOD group. NLRP3, nucleotide binding oligomerization domain-like receptor protein 3; caspase-1, cysteinyl aspartate specific proteinase-1; Ox-mtDNA, oxidized mitochondrial DNA; 8-OHdG, 8-hydroxy-desoxyguanosine.</p>
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<p>PCELNs alleviated HFD-induced MAFLD by promoting mitophagy and inhibiting NLRP3 inflammasome activation. PCELNs, <span class="html-italic">Poria cocos</span>-derived. ELNs; Ox-mtDNA, oxidized mitochondrial DNA.</p>
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15 pages, 3140 KiB  
Article
Role of Vanin-1 Gene Methylation in Fat Synthesis in Goose Liver: Effects of Betaine and 5-Azacytidine Treatments
by Xinfang Wang, Yu Shao, Zhi Yang, Haiming Yang and Zhiyue Wang
Animals 2025, 15(5), 719; https://doi.org/10.3390/ani15050719 - 3 Mar 2025
Viewed by 201
Abstract
This study aimed to investigate the mediating effect of vanin-1 (VNN1) and its DNA methylation on the reduction in liver fat synthesis due to the role of betaine and 5-Azacytidine (5-AZA) in geese. Twenty-eight 35-day-old male Jiangnan white geese with similar body weight [...] Read more.
This study aimed to investigate the mediating effect of vanin-1 (VNN1) and its DNA methylation on the reduction in liver fat synthesis due to the role of betaine and 5-Azacytidine (5-AZA) in geese. Twenty-eight 35-day-old male Jiangnan white geese with similar body weight (BW) and good health conditions were randomized into four groups (seven birds per group). All the birds were housed with the same type of basal diet. The control group was treated with normal saline intraperitoneally (I.P.); the AZA group was treated I.P. with AZA (2 mg/kg); the betaine group was fed with betaine through the diet and treated I.P. with normal saline (1.2 g/kg); the AZA+betaine group was fed with betaine through the diet and treated I.P. with AZA. The results showed that the administration of AZA significantly increased serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and VNN1 enzyme activity (p < 0.05); additionally, the expression levels of the molecules in various tissues were up-regulated to different extents, such as VNN1, fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), stearoyl-CoA dehydrogenase (SCD), and sterol regulatory element binding protein (SREBP); in contrast, the treatment of betaine reduced serum TC levels and the S-adenosylmethionine/S-adenosylhomocysteine (SAM/SAH) ratio; furthermore, hepatic DNA methylation in the AZA group was decreased in terms of the VNN1 promoter region. The results demonstrated that the expression of the VNN1 gene was negatively correlated with DNA methylation. This finding verified the key role of VNN1 and its methylation in the inhibition of liver lipid synthesis by betaine and provided a novel molecular mechanism for the regulation of liver lipid metabolism. Full article
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<p>Effects of different supplemental treatments on the body weight of geese from 35 to 49 days of age. (1) The control group was treated with normal saline intraperitoneally (I.P.); the AZA group was treated I.P. with AZA (2 mg/kg); the betaine group was fed with betaine through the diet and treated I.P. with normal saline (1.2 g/kg); the AZA+betaine group was fed with betaine through the diet and treated I.P. with AZA. (2) Values are presented as means and standard error of the means (<span class="html-italic">n</span> = 7). Values followed by different letters superscript indicate significant differences (<span class="html-italic">p</span> &lt; 0.05).</p>
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<p>(<b>A</b>): Effects of different treatment groups on lipid morphology of geese liver. (<b>B</b>): The proportion of lipid droplet area in different treatment groups. (1) The control group was treated with normal saline intraperitoneally (I.P.); the AZA group was treated I.P. with AZA (2 mg/kg); the betaine group was fed with betaine through the diet and treated I.P. with normal saline (1.2 g/kg); the AZA+betaine group was fed with betaine through the diet and treated I.P. with AZA; (2) HE staining of liver lipid (40×); (3) each group contains 3 individuals. The mean± SEM is presented for each group (<span class="html-italic">n</span> = 3).</p>
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<p>Effects of different treatments on DNA methylation level in VNN1 promoter region of gosling liver. (1) The control group was treated with normal saline intraperitoneally (I.P.); the AZA group was treated I.P. with AZA (2 mg/kg); the betaine group was fed with betaine through the diet and treated I.P. with normal saline (1.2 g/kg); the AZA+betaine group was fed with betaine through the diet and treated I.P. with AZA. (2) Closed and open circles represent methylated and unmethylated cytosines, respectively. Each bar represents the methylation level of the CpG site. Methylation at each CpG site of the promoter region was calculated by analyzing 10 clones.</p>
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<p>Effects of different treatment groups on the expression of <span class="html-italic">VNN1</span>, <span class="html-italic">FAS</span>, <span class="html-italic">ACC</span>, <span class="html-italic">SCD</span>, and <span class="html-italic">SREBPQ</span> genes in various organs. (1) (<b>A</b>) Effects of different treatments on the expression of VNN1 gene in the liver; (<b>B</b>) effects of different treatments on the expression of FAS gene in the kidney; (<b>C</b>) effects of different treatments on the expression of ACC gene in the heart; (<b>D</b>) effects of different treatments on the expression of SCD gene in the lung; (<b>E</b>) effects of different treatments on the expression of SREBPQ gene in the spleen; (2) values are presented as means and standard error of the means (<span class="html-italic">n</span> = 7). Values followed by different letters superscript indicate significant differences (<span class="html-italic">p</span> &lt; 0.05).</p>
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<p>Effects of different treatment groups on the expression of <span class="html-italic">VNN1</span>, <span class="html-italic">FAS</span>, <span class="html-italic">ACC</span>, <span class="html-italic">SCD</span>, and <span class="html-italic">SREBPQ</span> genes in various organs. (1) (<b>A</b>) Effects of different treatments on the expression of VNN1 gene in the liver; (<b>B</b>) effects of different treatments on the expression of FAS gene in the kidney; (<b>C</b>) effects of different treatments on the expression of ACC gene in the heart; (<b>D</b>) effects of different treatments on the expression of SCD gene in the lung; (<b>E</b>) effects of different treatments on the expression of SREBPQ gene in the spleen; (2) values are presented as means and standard error of the means (<span class="html-italic">n</span> = 7). Values followed by different letters superscript indicate significant differences (<span class="html-italic">p</span> &lt; 0.05).</p>
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17 pages, 4374 KiB  
Article
Lactobacillus fermentum 166, Derived from Yak Yogurt from Tibetan Areas of Sichuan, Improves High-Fat-Diet-Induced Hyperlipidemia by Modulating Gut Microbiota and Liver- and Gut-Related Pathways
by Shiqi Zhang, Limei Xu, Chenglin Zhu, Jing Li, Yu Fu, Weiming Shuang and Lianhong Chen
Foods 2025, 14(5), 867; https://doi.org/10.3390/foods14050867 - 3 Mar 2025
Viewed by 174
Abstract
The consumption of an unbalanced diet, such as a high-fat diet, is strongly associated with hyperlipidemia and significantly contributes to the development of cardiovascular and cerebrovascular diseases, which are the leading causes of death worldwide. Globally, about 17.9 million people die of cardiovascular [...] Read more.
The consumption of an unbalanced diet, such as a high-fat diet, is strongly associated with hyperlipidemia and significantly contributes to the development of cardiovascular and cerebrovascular diseases, which are the leading causes of death worldwide. Globally, about 17.9 million people die of cardiovascular disease each year (WHO 2023). Probiotics have emerged as a promising intervention to alleviate hyperlipidemia. Therefore, this study investigates the effects of Lactobacillus fermentum 166 (LF-166), isolated from yak yogurt in the Sichuan Tibetan area, on lipid metabolism in the liver and gut microbiota of high-fat-diet-induced hyperlipidemic mice. The results revealed that the Lactobacillus fermentum 166 (LF-166) treatment reduced the body weight and decreased the blood and liver lipid levels in these mice. Based on the histopathological findings, LF-166 could alleviate liver steatosis and colon injury. Additionally, 16S rRNA sequencing of the mice’s colonic contents showed that LF-166 reduced the Firmicutes/Bacteroidetes (F/B) value and enhanced the richness and diversity of the gut microbiota. LF-166 regulated hepatic lipid metabolism through the up-regulation of the genes Lxr, Ampkα, Fxr, Hsl, and Atgl and the down-regulation of C/ebpα and Pparγ in the liver; it also regulated intestinal lipid metabolism by up-regulating Abcg5 and Abcg8 in the ileum and down-regulating the expression of the genes Npc1l1, Asbt, and Ibabp. Thus, LF-166 may inhibit hyperlipidemia progression by modulating the expression of key genes involved in hepatic lipid metabolism, influencing the intestinal microbiota through the liver–gut axis, and regulating systemic lipid metabolism. Full article
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<p>Experimental design (14 weeks).</p>
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<p>Effect of LF-166 on body weight gain in mice. Data are presented as the mean ± standard deviation (<span class="html-italic">n</span> = 7/group). Repeated measures ANOVA for time and treatment effects includes time as a repeated measure and treatment group as a factor. Sample data in each group have a normal distribution. Difference in variance between the two groups was significant (<span class="html-italic">p</span> &lt; 0.05). <sup>a–d</sup> Mean values with different letters are significantly different (<span class="html-italic">p</span> &lt; 0.05) according to Tukey’s honestly significant difference test.</p>
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<p>Effects of LF-166 on lipid levels in mice. Total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels in serum of mice (<span class="html-italic">n</span> = 7). Data presented are the mean ± standard deviation (<span class="html-italic">n</span> = 7/group). Sample data in each group have a normal distribution. Difference in variance between the two groups is significant (<span class="html-italic">p</span> &lt; 0.05). <sup>a–e</sup> Mean values with different letters over the same column are significantly different (<span class="html-italic">p</span> &lt; 0.05) according to Tukey’s honestly significant difference test.</p>
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<p>(100×) H&amp;E pathological observation of liver and colon tissue in mice: (1) standard control diet group (CK); (2) HFD group (MG); (3) HFD + simvastatin group (DG); (4) HFD + low-dose LF-166 (10<sup>8</sup> CFU/mL) group (LD); (5) HFD + medium-dose LF-166 (MD); (6) HFD + high-dose LF-166 (HD); and (7) control diet + high-dose LF-166 (CK-166).</p>
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<p><span class="html-italic">Lxr</span> (<b>A</b>), <span class="html-italic">C</span>/<span class="html-italic">ebpα</span> (<b>B</b>), <span class="html-italic">Pparγ</span> (<b>C</b>), <span class="html-italic">Ampkα</span> (<b>D</b>), <span class="html-italic">Fxr</span> (<b>E</b>), <span class="html-italic">Srebp1</span> (<b>F</b>), <span class="html-italic">Hsl</span> (<b>G</b>), and <span class="html-italic">Atg</span> (<b>H</b>) mRNA expression in hepatic tissue of mice. Sample data in each group have a normal distribution, and the difference in variance between the two groups is significant (<span class="html-italic">p</span> &lt; 0.05). <sup>a–d</sup> Mean values with different letters in the bar are significantly different (<span class="html-italic">p</span> &lt; 0.05) according to Tukey’s honestly significant difference test.</p>
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<p><span class="html-italic">Asbt</span> (<b>A</b>), <span class="html-italic">Ibabp</span> (<b>B</b>), <span class="html-italic">Abcg5</span> (<b>C</b>), <span class="html-italic">Abcg8</span> (<b>D</b>), and <span class="html-italic">Npc1l1</span> (<b>E</b>) mRNA expression in the small intestine of mice. Sample data in each group have a normal distribution, and the difference in variance between the two groups is significant (<span class="html-italic">p</span> &lt; 0.05). <sup>a–d</sup> Mean values with different letters in the bar are significantly different (<span class="html-italic">p</span> &lt; 0.05) according to Tukey’s honestly significant difference test.</p>
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<p>Venn diagram of shared OTUs of six samples: (1) standard control diet group (CK); (2) HFD group (MG); (3) HFD + simvastatin group (DG); (4) HFD + low-dose LF-166 (10<sup>8</sup> CFU/mL) group (LD); (5) HFD + medium-dose LF-166 (MD); (6) HFD + high-dose LF-166 (HD); and (7) control diet + high-dose LF-166 (CK-166).</p>
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<p>Effect of IF-166 on Alpha diversity: (1) standard control diet group (CK); (2) HFD group (MG); (3) HFD + simvastatin group (DG); (4) HFD + low-dose LF-166 (10<sup>8</sup> CFU/mL) group (LD); (5) HFD + medium-dose LF-166 (MD); and (6) HFD + high-dose LF-166 (HD). Sample data in each group have a normal distribution, and the difference in variance between the two groups is significant (<span class="html-italic">p</span> &lt; 0.05). <sup>a–d</sup> Mean values with different letters in the bar are significantly different (<span class="html-italic">p</span> &lt; 0.05) according to Tukey’s honestly significant difference test.</p>
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<p>Impact of IF-166 on species distribution maps at the gate level: (1) standard control diet group (CK); (2) HFD group (MG); (3) HFD + simvastatin group (DG); (4) HFD + low-dose LF-166 (10<sup>8</sup> CFU/mL) group (LD); (5) HFD + medium-dose LF-166 (MD); (6) HFD + high-dose LF-166 (HD); and (7) control diet + high-dose LF-166 (CK-166).</p>
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<p>PCoA analysis of OTU level.</p>
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12 pages, 671 KiB  
Article
Adaptations of the Autonomic Nervous System and Body Composition After 8 Weeks of Specific Training and Nutritional Re-Education in Amateur Muay Thai Fighters: A Clinical Trial
by Antonio Beira de Andrade Junior, Elena Marie Peixoto Ruthes de Andrade, Guilherme Rodrigues de Souza and Agnaldo José Lopes
Sports 2025, 13(3), 72; https://doi.org/10.3390/sports13030072 - 3 Mar 2025
Viewed by 190
Abstract
Background: Considering that the nervous system regulates cardiac autonomic modulation (CAM) and that low CAM is associated with poorer performance, it is essential to evaluate the effects of training to increase parasympathetic modulation in Muay Thai (MT) fighters. Therefore, the aim of this [...] Read more.
Background: Considering that the nervous system regulates cardiac autonomic modulation (CAM) and that low CAM is associated with poorer performance, it is essential to evaluate the effects of training to increase parasympathetic modulation in Muay Thai (MT) fighters. Therefore, the aim of this study was to evaluate the effects of an 8-week intervention based on strength training and nutritional counseling on performance, CAM, and nutritional status in amateur MT fighters. Methods: This is a longitudinal and interventional study in which 22 MT fighters underwent a strength training program and nutritional protocol. Before and after the intervention, they underwent the ten-second frequency speed of kick test (FSKT-10s), multiple frequency speed of kick test (FSKT-mult), bioimpedance analysis (BIA), and assessment of heart rate variability. Results: After the intervention, there was an increase in the number of kicks in both FSKT-10s and FSKT-mult (p = 0.0008 and p = 0.032, respectively). In BIA, there was a significant increase in both fat-free mass and basal metabolic rate (p = 0.031 and p = 0.020, respectively). After the intervention, significant increases were observed during the physical test in the following variables that denote improvement in parasympathetic modulation: square root of the mean squared differences of successive RR intervals (p = 0.005); percentage of adjacent RR intervals with a difference in duration greater than 50 ms (p = 0.002); high frequency range (p < 0.0001); and standard deviation measuring the dispersion of points in the plot perpendicular to the line of identity (p = 0.004). Conclusions: In amateur MT fighters, an intervention with strength training and nutritional guidance is able to improve CAM through greater parasympathetic activation. Furthermore, there is an improvement in performance and body composition after the intervention. Full article
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<p>Comparisons of (<b>A</b>) the high frequency range (HF, <span class="html-italic">p</span> &lt; 0.0001) and (<b>B</b>) the standard deviation measuring the dispersion of points in the plot perpendicular to the line of identity (SD1, <span class="html-italic">p</span> = 0.001) obtained at rest before physical test between pre- and post-intervention. Data represent median (quartiles). Circles below or above the box plot indicate outliers.</p>
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<p>Comparisons of (<b>A</b>) square root of the mean squared differences of successive RR intervals (rMSSD, <span class="html-italic">p</span> = 0.005), (<b>B</b>) the percentage of adjacent RR intervals with a difference in duration greater than 50 ms (pNN50, <span class="html-italic">p</span> = 0.002), (<b>C</b>) the high frequency range (HF, <span class="html-italic">p</span> &lt; 0.0001), and (<b>D</b>) the standard deviation measuring the dispersion of points in the plot perpendicular to the line of identity (SD1, <span class="html-italic">p</span> = 0.004) obtained during the physical test between pre- and post-intervention. Data represent median (quartiles). Circles or stars below or above the box plot indicate outliers.</p>
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17 pages, 3348 KiB  
Article
Effects of Liupao Tea with Different Years of Aging on Glycolipid Metabolism, Body Composition, and Gut Microbiota in Adults with Obesity or Overweight: A Randomized, Double-Blind Study
by Yuyang Wang, Qiang Hu, Botian Chen and Defu Ma
Foods 2025, 14(5), 866; https://doi.org/10.3390/foods14050866 - 3 Mar 2025
Viewed by 161
Abstract
Background: Liupao tea (LPT) is a traditionally fermented dark tea from Guangxi, China and the effects of different aging periods of LPT on metabolic health remain inadequately explored. Methods: This randomized, double-blind, longitudinal study enrolled 106 adults with obesity or overweight who were [...] Read more.
Background: Liupao tea (LPT) is a traditionally fermented dark tea from Guangxi, China and the effects of different aging periods of LPT on metabolic health remain inadequately explored. Methods: This randomized, double-blind, longitudinal study enrolled 106 adults with obesity or overweight who were assigned to consume LPT of different ages over a 90-day period. Participants were randomly divided into four groups, each consuming LPT that had been aged for 1 year, 4 years, 7 years, or 10 years. The metabolic parameters, body composition, and gut microbiota were assessed at baseline and after the 90-day intervention. Results: All LPT groups experienced significant reductions in systolic blood pressure (SBP) and diastolic blood pressure (DBP), with the 10-year-aged group showing the most notable SBP decrease (p < 0.001). Total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels decreased significantly in the 1-, 4-, and 10-year-aged groups (p < 0.05), while high-density lipoprotein cholesterol (HDL-C) increased in the 7-year-aged group (p < 0.05). Body weight, body fat mass (BFM), body mass index (BMI), waist circumference (WC), body fat percentage (BFP), and visceral fat area (VFA) significantly declined across all groups (p < 0.05). Gut microbiota analysis showed changes in specific genera, though overall diversity remained stable. No significant differences were found in metabolic or microbiota outcomes between the different aged groups. Conclusions: LPT consumption effectively improves blood pressure, lipid profiles, and body composition in adults with obesity without adverse liver effects. The aging duration of LPT does not significantly alter these health benefits, challenging the belief that longer-aged LPT is superior. Full article
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<p>Study flowchart from participant recruitment to data analysis.</p>
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<p>Principal coordinate analysis (PCoA) and alpha diversity of gut microbiota across four LPT groups with different years of aging. (<b>a</b>) PCoA plots showed the differences in gut microbiota structure before and after intervention in the 1-year, 4-year, 7-year, and 10-year-aged groups. (<b>b</b>) Box plots of Shannon, Simpson, and Chao1 indices measuring alpha diversity in the four groups.</p>
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<p>Changes in the relative abundance of gut microbiota at the phylum (<b>a</b>) and genus (<b>b</b>) levels before and after intervention with LPT of different years of aging.</p>
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<p>Analysis of the gut bacteria at the genus level in LPT groups with different years of aging (only showing results with statistical significance). (<b>a</b>) 1-year-aged group; (<b>b</b>) 4-year-aged group; (<b>c</b>) 7-year-aged group; (<b>d</b>) 10-year-aged group.</p>
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20 pages, 14515 KiB  
Article
Hepatic Deletion of Carbohydrate Response Element Binding Protein Impairs Hepatocarcinogenesis in a High-Fat Diet-Induced Mouse Model
by Majedul Karim, Jessica Prey, Franziska Willer, Helen Leiner, Mohd Yasser, Frank Dombrowski and Silvia Ribback
Int. J. Mol. Sci. 2025, 26(5), 2246; https://doi.org/10.3390/ijms26052246 - 3 Mar 2025
Viewed by 155
Abstract
The transcription factor carbohydrate response element binding protein (ChREBP) has emerged as a crucial regulator of hepatic glucose and lipid metabolism. The increased ChREBP activity involves the pro-oncogenic PI3K/AKT/mTOR signaling pathway that induces aberrant lipogenesis, thereby promoting hepatocellular carcinomas (HCC). However, the molecular [...] Read more.
The transcription factor carbohydrate response element binding protein (ChREBP) has emerged as a crucial regulator of hepatic glucose and lipid metabolism. The increased ChREBP activity involves the pro-oncogenic PI3K/AKT/mTOR signaling pathway that induces aberrant lipogenesis, thereby promoting hepatocellular carcinomas (HCC). However, the molecular pathogenesis of ChREBP-related hepatocarcinogenesis remains unexplored in the high-fat diet (HFD)-induced mouse model. Male C57BL/6J (WT) and liver-specific (L)-ChREBP-KO mice were maintained on either a HFD or a control diet for 12, 24, and 48 weeks, starting at the age of 4 weeks. At the end of the feeding period, mice were perfused, and liver tissues were formalin-fixed, paraffin-embedded, sectioned, and stained for histological and immunohistochemical analysis. Biochemical and gene expression analysis were conducted using serum and frozen liver tissue. Mice fed with HFD showed a significant increase (p < 0.05) in body weight from 8 weeks onwards compared to the control. WT and L-ChREBP-KO mice also demonstrated a significant increase (p < 0.05) in liver-to-body weight ratio in the 48-week HFD group. HFD mice exhibited a gradual rise in hepatic lipid accumulation over time, with 24-week mice showing a 20–30% increase in fat content, which further advanced to 80–100% fat accumulation at 48 weeks. Both dietary source and the increased expression of lipogenic pathways at transcriptional and protein levels induced steatosis and steatohepatitis in the HFD group. Moreover, WT mice on a HFD exhibited markedly higher inflammation compared to the L-ChREBP-KO mice. The enhanced lipogenesis, glycolysis, persistent inflammation, and activation of the AKT/mTOR pathway collectively resulted in significant metabolic disturbances, thereby promoting HCC development and progression in WT mice. In contrast, hepatic loss of ChREBP resulted in reduced hepatocyte proliferation in the HFD group, which significantly contributed to the impaired hepatocarcinogenesis and a reduced HCC occurrence in the L-ChREBP-KO mice. Our present study implicates that prolonged HFD feeding contributes to NAFLD/NASH, which in turn progresses to HCC development in WT mice. Collectively, hepatic ChREBP deletion ameliorates hepatic inflammation and metabolic alterations, thereby impairing NASH-driven hepatocarcinogenesis. Full article
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<p>HFD feeding resulted in diet-induced obesity and hepatomegaly in WT and L-ChREBP-KO mice over a 48-week period. (<b>A</b>) Body weight changes of mice over 48 weeks, starting at 4 weeks of age. (<b>B</b>) Percent change in body weight from baseline. (<b>C</b>) Gross morphology of liver in each group. (<b>D</b>) Changes in liver weight in each group over 48 weeks. (<b>E</b>) Liver-to-body weight ratio in each group ((<b>A</b>,<b>B</b>,<b>D</b>,<b>E</b>): <span class="html-italic">n</span> = 264 per group in HFD; <span class="html-italic">n</span> = 25 per group in control). Values of the data are expressed as mean ± SEM. Significant differences are indicated as follows: *** <span class="html-italic">p</span> &lt; 0.001 vs. the control group.</p>
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<p>Effect of diet and genotype on biochemical parameters. (<b>A</b>) Changes in blood glucose levels over a 48-week period among the groups (<span class="html-italic">n</span> = 264 per group in HFD; <span class="html-italic">n</span> = 25 per group in control). (<b>B</b>,<b>C</b>) Serum ALT and AST levels in WT and L-ChREBP-KO mice at the age of 48 weeks (<span class="html-italic">n</span> = 5–6 per group). AST: Aspartate Aminotransferase; ALT: Alanine Aminotransferase. (<b>D</b>–<b>F</b>) Hepatic glycogen, triglyceride, and total cholesterol levels in 48-week WT and L-ChREBP-KO mice (<span class="html-italic">n</span> = 4–6 per group). Values of the data are expressed as mean ± SEM. Significant differences are indicated as follows: * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001 vs. the control group.</p>
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<p>Effects of HFD on the expression of hepatic lipid metabolism-related genes in 48-week mice. (<b>A</b>–<b>C</b>) Expression of key genes (FASN, ACACA, and SCD1) involved in de novo. (<b>D</b>) Lipogenic transcription factor SREBP-1c expression in 48-week mice. (<b>E</b>) Intracellular fat transport-associated gene CD36 expression in response to HFD feeding (<span class="html-italic">n</span> = 3–4 per group). Values of the data are expressed as mean ± SEM. Significant differences are indicated as follows: ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001 vs. the control group.</p>
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<p>Changes in expression levels of AKT1/mTOR, insulin signaling, glycolysis, and inflammation-associated genes in 48-week mice. (<b>A</b>,<b>B</b>) The mRNA expression of AKT1 and mTOR in 48-week mice. (<b>C</b>) Insulin signaling gene expression levels. (<b>D</b>) Altered expression of PKM2; (<b>E</b>,<b>F</b>) Upregulation of inflammation-related genes, TNFalpha and IL6 (<span class="html-italic">n</span> = 3–4 per group). Values of the data are expressed as mean ± SEM. Significant differences are indicated as follows: ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001 vs. the control group.</p>
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<p>Histological assessment of NAFLD/NASH at 48 weeks in WT and L-ChREBP-KO mice. (<b>A</b>) Histological scoring of HFD-induced steatosis at 48 weeks within each group (<span class="html-italic">n</span> = 264 per group in HFD; <span class="html-italic">n</span> = 25 per group in control). (<b>B</b>) HFD feeding led to inflammation in mice at 48 weeks within each group (<span class="html-italic">n</span> = 264 per group in HFD; <span class="html-italic">n</span> = 25 per group in control). (<b>C</b>) NAFLD scores at 48 weeks within each group of mice (<span class="html-italic">n</span> = 264 per group in HFD; <span class="html-italic">n</span> = 25 per group in control). (<b>D</b>) Representative images of H&amp;E-stained histological slides illustrating the enhanced fat accumulation in mice in response to HFD exposure. The black arrow in WT and L-ChREBP-KO indicates steatohepatitis in the HFD group. Scale bar: 100 µm. Values of the data are expressed as mean ± SEM. Significant differences are indicated as follows: *** <span class="html-italic">p</span> &lt; 0.001 vs. the control group.</p>
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<p>Representative images of immunohistochemical staining in liver tissue of WT and L-ChREBP-KO mice at 48 weeks. Activation of AKT/mTOR pathway in WT. Alteration in the expression of HK2, PKM2, and IRS1 in WT mice. Upregulation of de novo lipogenesis candidates FASN expression in WT mice. Scale bar: 100 µm.</p>
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<p>Tumor development, hepatocyte proliferation activity, and histological staining of WT and L-ChREBP-KO mice. (<b>A</b>) Representative macroscopic appearance of the liver with HCA and HCC in WT and L-ChREBP-KO mice. The red circle marks the HCA and HCC development within liver. (<b>B</b>) Ki-67 proliferation index in tumor tissue of WT mice (<span class="html-italic">n</span> = 55 in WT normal liver; <span class="html-italic">n</span> = 4 in WT tumor). The proliferation index for the L-ChREBP-KO HFD group was excluded from statistical analysis because only one tumor was observed in this group. (<b>C</b>) Representative immunohistochemical image with Ki-67 staining in WT HFD and WT HFD tumor tissue. The proliferation index of Ki-67-stained hepatocytes was determined at 40× magnification and the nuclei were counted in three randomly chosen fields, which was approximately 2000 cells per section. Positive hepatocytes for Ki-67 are stained in brown. (<b>D</b>) H&amp;E staining of WT and L-ChREBP-KO mice. The black dashed line demarcates HCC development from normal liver (left picture). Magnifications for H&amp;E staining: 10×, 40×, and 100×. Scale bar: 1000 µm for 10× and 100 µm for 40× and 100×. Values of the data are expressed as mean ± SEM. Significant differences are indicated as follows: *** <span class="html-italic">p</span> &lt; 0.001 vs. the control group.</p>
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<p>Representative immunohistochemical staining in HCC tissue of WT and L-ChREBP-KO mice. Alteration in the expression of HK2, PKM2 and IRS1 in WT. Upregulated expression of pAKT, pmTOR, and p4EBP1 in WT. Increased expression of de novo lipogenesis proteins, ACAC, and FASN, in WT mice. Scale bar: 100 µm.</p>
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10 pages, 205 KiB  
Article
Association Between Anthropometric Measurements and Mediterranean Lifestyle in Women Diagnosed with Hashimoto’s Thyroiditis: Data from the Mediterranean Region
by Burcin Karavelioglu, Taygun Dayi, Osman Koseoglulari and Adile Oniz
Nutrients 2025, 17(5), 892; https://doi.org/10.3390/nu17050892 - 3 Mar 2025
Viewed by 157
Abstract
Background/Objectives: Hashimoto’s thyroiditis (HT) is the most common autoimmune disease which lowers a patient’s quality of life. Our study aimed to assess the association between Mediterranean lifestyle and anthropometric measurements in patients with HT. Methods: This study was conducted with 120 female patients [...] Read more.
Background/Objectives: Hashimoto’s thyroiditis (HT) is the most common autoimmune disease which lowers a patient’s quality of life. Our study aimed to assess the association between Mediterranean lifestyle and anthropometric measurements in patients with HT. Methods: This study was conducted with 120 female patients previously diagnosed with HT. The ‘Mediterranean Diet Adherence Screener-(MEDAS)’ and ‘MEDiterranean LIFEstyle-(MEDLIFE)’ scales were used to assess diet quality and lifestyle. Also, some anthropometric measurements were collected. Spearman’s Correlation Test was used to determine correlations between two quantitative variables. Results: The average age of the participants was 37.49 ± 7.47 years. The average diet quality scores were 7.80 ± 1.93 for MEDAS and the total life quality score was 16.41 ± 3.74 for MEDLIFE. Significant negative correlations were observed between the MEDLIFE total score and hip and waist circumferences, body weight, and body fat (%) (p < 0.05), as well as with the score of physical activity, rest, social habits, and conviviality (p < 0.05). Furthermore, an increase the Mediterranean dietary habits score was associated with a decrease in these measurements (p < 0.05). Conclusions: The MEDLIFE score, beyond only the Mediterranean dietary habits sub-score, was found to be associated with lower anthropometric measurements in patients with HT, who are at higher risk of pre-obesity and obesity. Full article
(This article belongs to the Section Nutrition in Women)
19 pages, 5049 KiB  
Article
Graphene-Based Far-Infrared Therapy Promotes Adipose Tissue Thermogenesis and UCP1 Activation to Combat Obesity in Mice
by Jinshui Zhang, Shuo Li, Xin Cheng, Xiaocui Tan, Yingxian Shi, Guixin Su, Yulong Huang, Yang Zhang, Rui Xue, Jingcao Li, Qiongyin Fan, Huajin Dong, Yun Deng and Youzhi Zhang
Int. J. Mol. Sci. 2025, 26(5), 2225; https://doi.org/10.3390/ijms26052225 - 28 Feb 2025
Viewed by 255
Abstract
Hyperthermia (HT) has broad potential for disease treatment and health maintenance. Previous studies have shown that far-infrared rays (FIRs) at 8–10 μm can potentially reduce inflammation, oxidative stress, and gut microbiota imbalance. However, the effects of FIR HT on energy metabolism require further [...] Read more.
Hyperthermia (HT) has broad potential for disease treatment and health maintenance. Previous studies have shown that far-infrared rays (FIRs) at 8–10 μm can potentially reduce inflammation, oxidative stress, and gut microbiota imbalance. However, the effects of FIR HT on energy metabolism require further investigation. To investigate the effects of graphene-FIR HT therapy on diet-induced obesity and their regulatory mechanisms in energy metabolism disorders. After 8 weeks of hyperthermia, mice fed standard chow or a high-fat diet (HFD) underwent body composition analysis. Energy expenditure was measured using metabolic cages. The protein changes in adipose tissue were detected by molecular technology. Graphene-FIR therapy effectively mitigated body fat accumulation, improved dyslipidemia, and impaired liver function while enhancing insulin sensitivity. Furthermore, graphene-FIR therapy increased VO2, VCO2, and EE levels in HFD mice to exhibit enhanced metabolic activity. The therapy activated the AMPK/PGC-1α/SIRT1 pathway in adipose tissue, increasing the expression of uncoupling protein 1 (UCP1) and glucose transporter protein four (GLUT4), activating the thermogenic program in adipose tissue, and improving energy metabolism disorder in HFD mice. In short, graphene-FIR therapy represents a comprehensive approach to improving the metabolic health of HFD mice. Full article
(This article belongs to the Section Molecular Endocrinology and Metabolism)
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<p>Specific FIR generated by graphene-based devices. (<b>A</b>) SEM image of graphene film; (<b>B</b>) Raman spectrum of the graphene FIR; (<b>C</b>) SEM image of carbon fiber film; (<b>D</b>) Raman spectrum of the carbon fiber FIR; (<b>E</b>) FIR emission spectra of graphene and carbon fiber (graphene: 30 W, carbon fiber: 30 W); (<b>F</b>) the absorption peak of the human body surface was approximately 8.0 µm; (<b>G</b>) the FIR emission peak of the graphene was approximately 8.03 µm, and the carbon fiber was approximately 7.685 µm.</p>
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<p>Graphene-FIR therapy induces thermogenesis and increases blood flow in vivo. (<b>A</b>) Schematic representation of thermal imaging of human supraclavicular area and temperature changes before or after Gra-FIR therapy. Data are displayed as mean ± SEM; <span class="html-italic">n</span> = 10, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 VS baseline. The selected part of the black box is the temperature detection area. (<b>B</b>,<b>C</b>) Schematic diagram of thermal imaging and statistical analysis of temperature changes in mice after Gra-FIR or Car-FIR. (<b>D</b>–<b>F</b>) A schematic diagram of rectal temperature measurement in mice and statistical analysis of rectal temperature changes before and after the Gra-FIR or Car-FIR therapy. (<b>G</b>–<b>I</b>) Representative images and statistical analysis of blood perfusion in BAT and iWAT of mice after Gra-FIR or Car-FIR therapy. The site selected by the black circle box was the blood flow detection area. Data are displayed as mean ± SEM; <span class="html-italic">n</span> = 7, ** <span class="html-italic">p</span> &lt; 0.01 VS NC group; <sup>##</sup> <span class="html-italic">p</span> &lt; 0.01 VS Gra-FIR group.</p>
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<p>Graphene-FIR therapy can improve HFD-induced weight gain. (<b>A</b>) Schematic of the experimental design. (<b>B</b>) Schematic diagram of the FIR device. (<b>C</b>) Line chart of mice body weight in each group (<span class="html-italic">n</span> = 7–10). (<b>D</b>) The total body fat and mass content of each group (<span class="html-italic">n</span> = 6). (<b>E</b>) Representative images of liver, BAT, and iWAT in each group. (<b>F</b>) Organ weight in each group (<span class="html-italic">n</span> = 7–10). (<b>G</b>) HE staining of liver, BAT, and iWAT (200X; <span class="html-italic">n</span> = 3). Scale-bar: 50 μm. Data are displayed as mean ± SEM. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 VS NC group; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05, <sup>##</sup> <span class="html-italic">p</span> &lt; 0.01 VS HFD group.</p>
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<p>Graphene-FIR therapy can improve dyslipidemia and insulin resistance in HFD mice. (<b>A</b>–<b>F</b>) The serum levels of TG, TC, LDL-C, HDL-C, ALT, and AST. (<b>G</b>,<b>H</b>) GTT and area under the curve. (<b>I</b>,<b>J</b>) ITT and area under the curve. (<b>K</b>) Fasting blood glucose levels. (<b>L</b>–<b>N</b>) Serum levels of leptin, insulin, and adiponectin. (<b>O</b>) HOMA-IR index. Data are displayed as mean ± SEM; <span class="html-italic">n</span> = 6–10, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05, <sup>##</sup> <span class="html-italic">p</span> &lt; 0.01 VS HFD group.</p>
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<p>Graphene-FIR therapy has no impact on energy intake but increases EE in HFD mice, (<b>A</b>,<b>B</b>) Daily food intake of each group. (<b>C</b>) Energy intake of mice. (<b>D</b>,<b>E</b>) O<sub>2</sub> consumption (V<sub>O2</sub>). (<b>F</b>,<b>G</b>) CO<sub>2</sub> release (V<sub>CO2</sub>). (<b>H</b>,<b>I</b>) Energy expenditure. (<b>J</b>,<b>K</b>) Respiratory exchange rate (RER). (<b>L</b>) Core temperature. (<b>M</b>–<b>P</b>) Predicted metabolic rate (MR) either in light or dark. (<b>Q</b>,<b>R</b>) Activity distance within 24 h. (<b>S</b>,<b>T</b>) Number of activities within 24 h. Data are displayed as mean ± SEM; <span class="html-italic">n</span> = 6–10, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, ns represents no significant difference.</p>
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<p>Graphene-FIR therapy could activate adipose tissue thermogenesis and activate the AMPK/SIRT1/PGC-1α pathway in HFD mice. (<b>A</b>–<b>E</b>) Representative protein bands and relative protein expressions of AMPK, PGC-1α, SIRT1, UCP1, and GLUT4. β-actin was used as a loading control. (<b>F</b>–<b>J</b>) The mRNA expression of thermogenic genes. Data are displayed as mean ± SEM; <span class="html-italic">n</span> = 6, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01.</p>
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20 pages, 2078 KiB  
Article
Associations Between Clinical Inflammatory Risk Markers, Body Composition, Heart Rate Variability, and Accelerometer-Assessed Physical Activity in University Students with Overweight and Obesity
by Sascha W. Hoffmann, Janis Schierbauer, Paul Zimmermann, Thomas Voit, Auguste Grothoff, Nadine Wachsmuth, Andreas Rössler, Tobias Niedrist, Helmut K. Lackner and Othmar Moser
Sensors 2025, 25(5), 1510; https://doi.org/10.3390/s25051510 - 28 Feb 2025
Viewed by 117
Abstract
This cross-sectional study aimed to identify associations between clinical inflammatory risk markers, body composition, heart rate variability (HRV), and self-reported and objectively assessed physical activity (PA) in university students with overweight and obesity. Seventeen participants (eight females) completed a screening visit following a [...] Read more.
This cross-sectional study aimed to identify associations between clinical inflammatory risk markers, body composition, heart rate variability (HRV), and self-reported and objectively assessed physical activity (PA) in university students with overweight and obesity. Seventeen participants (eight females) completed a screening visit following a randomized controlled four-arm crossover trial period with 8 h of uninterrupted prolonged sitting, alternate sitting and standing, continuous standing, and continuous slow walking, respectively. Clinical inflammatory risk markers were obtained from venous blood samples, and PA was assessed using the International Physical Activity Questionnaire (IPAQ-SF) and ActiGraph wGT3X-BT accelerometers. HRV was recorded over 24 h using the Faros 180 Holter electrocardiogram (ECG). White blood cell (WBC) counts were significantly correlated with fat mass (FM; p = 0.03) and visceral adipose tissue (VAT; p = 0.04) and inversely correlated with moderate PA (p = 0.02). Light-intensity PA (LIPA) and moderate-to-vigorous PA (MVPA) were correlated with HRV parameters (p = 0.02), and LIPA was inversely correlated with interleukin-6 (p = 0.003) and c-reactive protein (p = 0.04) during different trial conditions. In university students with overweight and obesity, higher values of FM were negatively correlated with WBC count, and integrating LIPA and MVPA in the students’ daily life strengthened their sympathetic–parasympathetic regulation and positively mediated anti-inflammatory mechanisms. Full article
(This article belongs to the Section Wearables)
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<p>Participant flow chart. BIA, bioelectrical impedance analysis; OGTT, oral glucose tolerance test; BLOOD, venous blood sampling; QUE, questionnaire; HRV, heart rate variability; ACT, accelerometry with Actigraphy wGT3X-bt.</p>
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<p>Simple linear regression analyses with the respective regression lines (bold lines) and the 95% CIs (dotted lines) between clinical inflammatory markers, body composition parameters, and physical activity variables at the time of the screening visit. (<b>a</b>) Leucocytes and moderate physical activity (MPA); (<b>b</b>) Neutrophil granulocyte count and moderate physical activity (MPA); (<b>c</b>) Neutrophil granulocyte count and visceral adipose tissue area (VAT); (<b>d</b>) Immature granulocyte count and body mass index (BMI); (<b>e</b>) Immature granulocyte count and fat mass (FM); (<b>f</b>) Eosinophil granulocyte count and fat mass (FM); (<b>g</b>) Eosinophil granulocyte count and visceral adipose tissue area (VAT); (<b>h</b>) Basophilic granulocyte count and fat mass (FM); (<b>i</b>) Basophilic granulocyte count and visceral adipose tissue area (VAT).</p>
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<p>Simple linear regression analyses with the respective regression lines (bold lines) and the 95% CIs (dotted lines) between clinical inflammatory markers, body composition parameters, and physical activity variables at the time of the screening visit. (<b>a</b>) Leucocytes and moderate physical activity (MPA); (<b>b</b>) Neutrophil granulocyte count and moderate physical activity (MPA); (<b>c</b>) Neutrophil granulocyte count and visceral adipose tissue area (VAT); (<b>d</b>) Immature granulocyte count and body mass index (BMI); (<b>e</b>) Immature granulocyte count and fat mass (FM); (<b>f</b>) Eosinophil granulocyte count and fat mass (FM); (<b>g</b>) Eosinophil granulocyte count and visceral adipose tissue area (VAT); (<b>h</b>) Basophilic granulocyte count and fat mass (FM); (<b>i</b>) Basophilic granulocyte count and visceral adipose tissue area (VAT).</p>
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<p>Simple linear regression analyses with the respective regression lines (bold lines) and the 95% CIs (dotted lines) between heart rate variability parameters, inflammatory markers, and accelerometer-assessed physical activity variables during the trial period. (<b>a</b>) Standard deviation of normal-to-normal beat (SDNN) and moderate-to-vigorous physical activity (MVPA); (<b>b</b>) Root mean square of successive differences (RMSSD) and moderate-to-vigorous physical activity (MVPA); (<b>c</b>) High frequency (HF) and moderate-to-vigorous physical activity (MVPA); (<b>d</b>) High frequency (HF) and metabolic equivalent of task (MET); (<b>e</b>) High frequency (HF) and light-intensity physical activity (LIPA); (<b>f</b>) Interleukin-6 (IL-6) during the WALK condition and metabolic equivalent of task (MET); (<b>g</b>) Interleukin-6 (IL-6) during the WALK condition and light-intensity physical activity (LIPA); (<b>h</b>) Interleukin-6 (IL-6) during the SIT condition and vigorous physical activity (VPA); (<b>i</b>) C-reactive protein (CRP) during the STAND condition and light-intensity physical activity (LIPA).</p>
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15 pages, 470 KiB  
Article
Evaluation of Effect of Dietary Supplementation with Microencapsulated Hydrolyzed Tannins on Growth, Slaughter Performance, Meat Quality, and Lipid Metabolism of Zhongshan Shelducks
by Zhimei Tian, Zhengwei Tian, Yingshan Yin, Yongmei Wu, Zhenyuan Li, Qiaohua Liang, Miao Yu, Yiyan Cui, Xianyong Ma, Guanghui Peng and Zhenming Li
Foods 2025, 14(5), 839; https://doi.org/10.3390/foods14050839 - 28 Feb 2025
Viewed by 226
Abstract
This study investigated the effects of microenapsulated hydrolyzed tannins (MHTs) on the growth performance and meat quality of Zhongshan shelducks. A total of 288 healthy Zhongshan shelducks with an average initial weight of 1790.27 ± 0.14 kg were randomly divided into four groups [...] Read more.
This study investigated the effects of microenapsulated hydrolyzed tannins (MHTs) on the growth performance and meat quality of Zhongshan shelducks. A total of 288 healthy Zhongshan shelducks with an average initial weight of 1790.27 ± 0.14 kg were randomly divided into four groups through a 56 d experiment period and were fed a basal diet supplemented with 0 (CON), 400, 800, and 1600 mg/kg MHTs, respectively. Results showed that 400 and 800 mg/kg MHTs improved the final body weight, average daily gain, glutathione peroxidase activity, and total antioxidant capacity compared to CON (p ≤ 0.05). The diet supplemented with 400 mg/kg MHTs decreased shear force and 800 mg/kg MHTs increased the yield of pectoralis major muscle compared to CON (p ≤ 0.05). Dietary MHTs increased inosine monophosphate content and decreased percentage C14:0 content in meat; however, the b*45 min value, 48 h drip loss, and shear force were increased but the percentage intramuscular fat (IMF) content was decreased in pectoralis major muscle with the increase in MHTs (p ≤ 0.05). Compared to CON, 400 and 800 mg/kg MHTs increased the percentage content of IMF, C18:1n-9, C18:2n-6, monounsaturated fatty acids, polyunsaturated fatty acids, and unsaturated fatty acids in pectoralis major muscle (p ≤ 0.05). Furthermore, 400 and 800 mg/kg MHTs improved the lipid metabolism of IMF deposition, fatty acid uptake, and adipogenesis by activating the peroxisome proliferator-activated receptor gamma pathway to regulate fatty acid synthetase and lipoprotein lipase genes. In conclusion, diets supplemented with 400 and 800 mg/kg MHTs could improve growth, meat quality, antioxidant capacity, and lipid metabolism in Zhongshan shelducks. Full article
(This article belongs to the Section Meat)
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<p>Effects of MHTs on the expression of lipid metabolism-related genes in pectoralis major muscle in Zhongshan ducks. Dietary treatments of 0, 400, 800, and 1600 were basal diets supplemented with 0, 400, 800, and 1600 mg/kg MHTs, respectively. Values are shown as the mean ± SEM. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001. The results are presented as means and SEMs (<span class="html-italic">n</span> = 6). <span class="html-italic">ACC</span>, acetyl-coenzyme A carboxylase; <span class="html-italic">FAS</span>, fatty acid synthetase; <span class="html-italic">PPARα/γ</span>, peroxisome proliferator-activated receptor alpha/gamma; <span class="html-italic">ADPN</span>, adiponectin; <span class="html-italic">SREBP</span>-1, sterol regulatory element-binding protein 1; <span class="html-italic">LPL</span>, lipoprotein lipase; <span class="html-italic">SIRT</span>1, sirtuin 1; <span class="html-italic">FOXO</span>1, forkhead transcription factor.</p>
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13 pages, 240 KiB  
Article
Adenovirus 36 Seropositivity Is Related to Inflammation and Imbalance Between Oxidative Stress and Antioxidant Status Regardless of Body Mass Index in Mexican Population
by Omar Arroyo-Xochihua, Cristian Arbez-Evangelista, Edgar Miranda-Contreras, Yeimy Mar De León-Ramírez, Montserrat Díaz-Edgar, Clara Luz Sampieri, Omar Arroyo-Helguera and María Teresa Álvarez-Bañuelos
Curr. Issues Mol. Biol. 2025, 47(3), 166; https://doi.org/10.3390/cimb47030166 - 28 Feb 2025
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Abstract
Background: The etiology of obesity has been associated with genetic and epigenetic factors, hormonal changes, unhealthy lifestyle habits, and infectious agents such as human adenovirus-36 (HAdV-36). Viral infections induce reactive oxygen species, and the imbalance between oxidative stress/antioxidant results in fat accumulation. In [...] Read more.
Background: The etiology of obesity has been associated with genetic and epigenetic factors, hormonal changes, unhealthy lifestyle habits, and infectious agents such as human adenovirus-36 (HAdV-36). Viral infections induce reactive oxygen species, and the imbalance between oxidative stress/antioxidant results in fat accumulation. In the Mexican population, little is known about the frequency of HAdV-36 and its effect on the balance between antioxidants and oxidants, inflammation, and metabolic markers. The purpose of our study was to evaluate the frequency of HAdV-36 seroprevalence and its relation to body mass index (BMI), lipid profiles, glucose levels, inflammation, and levels of antioxidants and oxidative stress in a representative sample. A cross-sectional study was carried out on 112 healthy adults between 18 and 28 years old, who were divided into four groups according to their BMI: underweight (BMI < 18.5); normal weight (BMI 18.5–24.9); overweight (BMI ≥ 25); and obese (BMI ≥ 30). Blood samples were taken to evaluate lipid and glucose profiles, as well as antioxidant and oxidative stress status, using colorimetric techniques. Seropositivity for HAdV-36 and levels of TNF-α, IL-6, and cortisol were determined using an enzyme-linked immunosorbent assay. The HAdV-36 frequency was 15.6% in underweight subjects, 18.7% in the normal-weight subjects, 34.37% in the overweight subjects, and 31.24% in the obese subjects. The subjects who were positive for HAdV-36 seroprevalence had increased levels of IL-6, cortisol, and oxidative stress, independently of BMI. The HAdV-36-positive subjects had reduced LDL-C and HDL-C levels only in the low-weight groups. Glutathione and SOD levels increased in the underweight and normal-weight subjects with positive HAdV-36 seroprevalence, while catalase levels decreased in the normal-weight, overweight, and obese subjects. In conclusion, for the first time, an HAdV-36 seroprevalence in the adult Mexican population is reported which was higher and had a relation with the presence of inflammation, alterations in the lipid profile, and imbalance between oxidative stress and antioxidant status, regardless of BMI. The oxidative stress/antioxidant imbalance could be participating in the stimulation of white adipose tissue deposition. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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