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Non-alcoholic Fatty Liver Disease (NAFLD) and Obesity: Influence of the Diet, Impact of the Serum Lipid Profile and Nutritional Status

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: 25 February 2025 | Viewed by 7372

Special Issue Editor


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Guest Editor
1. Escuela Universitaria de Enfermería y Fisioterapia San Juan de Dios, Universidad Pontificia de Comillas, Madrid, Spain
2. Obesity Unit, Garcilaso Clinic, Madrid, Spain
Interests: obesity; bariatric surgery; liver disease; nutrition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity is associated with an increased risk of non-alcoholic fatty liver disease (NAFLD). Adipose tissue is subjected to a state of chronic inflammation capable of secreting adipokines. This has made it possible to establish an association between metabolic alterations leading to triglyceride accumulation and hepatic inflammation, and has reinforced the role of hepatocellular lipotoxicity in the pathogenesis of non-alcoholic fatty liver disease.

The type of diet a person eats has been shown to be associated not only with the development of obesity, but also with fat accumulation in the liver parenchyma independently of body adiposity. The gold standard for the diagnosis of NAFLD is liver biopsy, but since it is an invasive technique, it is not routinely performed. Therefore, a diagnosis of suspicion can be made via imaging tests (ultrasound, MR, elastography, etc.) or even biochemical markers that can be determined from a routine analysis.

Dr. Jaime Ruiz-Tovar
Guest Editor

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Keywords

  • liver steatosis
  • non-alcoholic fatty liver disease
  • NAFLD
  • obesity
  • body mass index
  • adipokines
  • diet

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Published Papers (5 papers)

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Research

16 pages, 1125 KiB  
Article
Impact of L-Citrulline Supplementation and HIIT on Lipid Profile, Arterial Stiffness, and Fat Mass in Obese Adolescents with Metabolic-Dysfunction-Associated Fatty Liver Disease: A Randomized Clinical Trial
by Alan Arturo Rodríguez-Carrillo, Mario Ramón Espinoza-Vargas, Katya Vargas-Ortiz, Lorena del Rocío Ibarra-Reynoso, Monserrat Olvera-Juárez, Armando Gómez-Ojeda, Ma. Eugenia Garay-Sevilla and Arturo Figueroa
Nutrients 2025, 17(3), 402; https://doi.org/10.3390/nu17030402 - 23 Jan 2025
Viewed by 980
Abstract
Background: Metabolic-dysfunction-associated steatotic liver disease (MASLD) and obesity contribute to vascular dysfunction through oxidative stress, heightening cardiovascular risk. Oral supplementation with L-citrulline (L-cit), a precursor of L-arginine (L-arg) and nitric oxide, and high-intensity interval training (HIIT) may improve vascular function and cardiometabolic health. [...] Read more.
Background: Metabolic-dysfunction-associated steatotic liver disease (MASLD) and obesity contribute to vascular dysfunction through oxidative stress, heightening cardiovascular risk. Oral supplementation with L-citrulline (L-cit), a precursor of L-arginine (L-arg) and nitric oxide, and high-intensity interval training (HIIT) may improve vascular function and cardiometabolic health. Objectives: This study aimed to evaluate the combined effects of L-cit supplementation and HIIT on arterial stiffness, body composition, glucose metabolism, lipid profile, and blood pressure (BP) in adolescents with MASLD and obesity. Methods: In this double-blind, placebo-controlled, randomized clinical trial (ClinicalTrials.gov (NCT05778266), 44 adolescents (15–19 years) with MASLD and obesity were assigned to HIIT + L-cit (n = 14), HIIT + placebo (n = 14), or L-cit (n = 15) for 12 weeks. HIIT sessions (85% and 60% peak heart rate during intense and recovery periods) occurred thrice weekly. Training volume progressively increased, and participants performed 20 min of HITT per session in the last 8 weeks. Results: Outcomes included pulse wave velocity (PWV), augmentation index (Aix75), VO2peak, body composition, BP, glucose and lipid profiles, and hepatic steatosis. Compared to L-cit, HIIT + L-cit improved non-high-density lipoprotein cholesterol (p = 0.04), very-low-density lipoprotein cholesterol (p = 0.01), triglycerides (p = 0.02), and VO2peak (p = 0.001). No significant between-group changes were found in PWV, AIx75, hepatic steatosis, and body composition. HIIT + placebo improved VO2peak (p = 0.002), and L-cit decreased the degree of steatosis (p = 0.038). Conclusions: HIIT + L-cit supplementation enhanced lipid profile and cardiorespiratory fitness, while HIIT + placebo improved cardiorespiratory capacity, and L-cit alone decreased hepatic steatosis. Thus, L-cit could be an adjuvant strategy to manage obesity-related MASLD in adolescents. Full article
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Graphical abstract

Graphical abstract
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<p>CONSORT flow diagram.</p>
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<p>NS: not significant; VO2peak: peak oxygen consumption; VLDL: very-low-density lipoprotein; HIIT: high-intensity interval training; L-cit: L-citrulline; Pla: placebo. Absolute changes in (<b>A</b>) VO2peak, (<b>B</b>) VLDL-C, (<b>C</b>) non-HDL-C, and (<b>D</b>) triglycerides after 12 weeks of intervention. Analysis performed with one-way ANOVA (blue) or the Kruskal–Wallis test (green) according to normality of data. Post hoc comparisons were conducted using the Bonferroni test: a: <span class="html-italic">p</span> &lt; 0.05 vs. L-cit; b: <span class="html-italic">p</span> &lt; 0.01 vs HIIT + placebo; c: <span class="html-italic">p</span> &lt; 0.01 vs. L-cit; d: <span class="html-italic">p</span> &lt; 0.05 vs. HIIT + placebo.</p>
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14 pages, 2315 KiB  
Article
No Difference in Liver Damage Induced by Isocaloric Fructose or Glucose in Mice with a High-Fat Diet
by Wei-Fan Hsu, Ming-Hsien Lee, Chong-Kuei Lii and Cheng-Yuan Peng
Nutrients 2024, 16(20), 3571; https://doi.org/10.3390/nu16203571 - 21 Oct 2024
Viewed by 1482
Abstract
Background/Objectives: The diverse effects of fructose and glucose on the progression of metabolic dysfunction-associated steatotic liver disease remain uncertain. This study investigated the effects, in animal models, of high-fat diets (HFDs) supplemented with either glucose or fructose. Methods: Six-week-old, male C57BL/6J [...] Read more.
Background/Objectives: The diverse effects of fructose and glucose on the progression of metabolic dysfunction-associated steatotic liver disease remain uncertain. This study investigated the effects, in animal models, of high-fat diets (HFDs) supplemented with either glucose or fructose. Methods: Six-week-old, male C57BL/6J mice were randomly allocated to four groups: normal diet (ND), HFD, HFD supplemented with fructose (30% w/v, HFD + Fru), and HFD supplemented with glucose (initially 30%, HFD + Glu). After 24 weeks, liver and plasma samples were gathered for analysis. In addition, 39 patients with obesity undergoing bariatric surgery with wedge liver biopsy were enrolled in the clinical study. Results: The HFD + Glu group consumed more water than did the HFD and HFD + Fru groups. Thus, we reduced the glucose concentration from 30% at baseline to 15% at week 2 and 10% starting from week 6. The HFD + Fru and HFD + Glu groups had a similar average caloric intake (p = 0.463). The HFD increased hepatic steatosis, plasma lipid levels, lipogenic enzymes, steatosis-related oxidative stress, hepatic inflammation, and early-stage liver fibrosis. Supplementation with fructose or glucose exacerbated liver damage, but no significant differences were identified between the two. The expression patterns of hepatic ceramides in HFD-fed mice (with or without supplemental fructose or glucose) were similar to those observed in patients with obesity and severe hepatic steatosis or metabolic dysfunction–associated steatohepatitis. Conclusions: Fructose and glucose similarly exacerbated liver damage when added to an HFD. Ceramides may be involved in the progression of hepatic lipotoxicity. Full article
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Figure 1
<p>Effects of HFD and HFD supplemented with fructose or glucose on body and liver weight, biochemical parameters, and liver histology. (<b>A</b>) Body weight (* <span class="html-italic">p</span> &lt; 0.05 compared with ND group). (<b>B</b>) Liver weight as a percentage of body weight. (<b>C</b>) ALT levels. (<b>D</b>) TG, T-chol, HDL-C, and LDL-C levels. (<b>E</b>) Insulin resistance. (<b>F</b>) Liver histology: hematoxylin and eosin staining (400×, upper panel), Masson’s trichrome staining (200×, lower panel), and NASH CRN score. ND, normal diet; HFD, high-fat diet; HFD + Fru, high-fat diet supplemented with fructose; HFD + Glu, high-fat diet supplemented with glucose; ALT, alanine aminotransferase; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment-insulin resistance; LDL-C, low-density lipoprotein cholesterol; NASH CRN, nonalcoholic steatohepatitis Clinical Research Network; T-chol, total cholesterol; TG, triglyceride. * <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.</p>
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<p>Effects of HFD and HFD supplemented with fructose or glucose on lipogenic enzymes, oxidative stress markers, and lipid peroxidation. (<b>A</b>) mRNA levels of SREBP-1c, ACC, and FAS. (<b>B</b>) Protein levels of SREBP-1c, ACC, FAS, and PPAR-α. (<b>C</b>) Protein levels of p-Nrf2, GCLM, GCLC, and GPX2. (<b>D</b>) Protein levels of SOD-2, HO-1, and catalase. (<b>E</b>) TBARS values. ND, normal diet; HFD, high-fat diet; HFD + Fru, high-fat diet supplemented with fructose; HFD + Glu, high-fat diet supplemented with glucose; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthase; GCLC, glutamate–cysteine ligase catalytic subunit; GCLM, glutamate–cysteine ligase modifier subunit; GPX2, glutathione peroxidase 2; HO-1, heme oxygenase 1; pNrf2, phosphorylated nuclear factor-erythroid 2; PPAR-α, peroxisome proliferator-activated receptor α; SOD-2, superoxide dismutase 2; SREBP-1c, sterol regulatory element-binding protein-1c; TBARS, thiobarbituric acid-reactive substance. * <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.</p>
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<p>Effects of HFD and HFD supplemented with fructose or glucose on hepatic apoptosis, inflammation, and fibrosis. (<b>A</b>) mRNA and protein levels of CHOP. (<b>B</b>) mRNA levels of TNF-α and NLRP3 and protein level of NLRP3. (<b>C</b>) Protein level of αSMA. ND, normal diet; HFD, high-fat diet; HFD + Fru, high-fat diet supplemented with fructose; HFD + Glu, high-fat diet supplemented with glucose; α-SMA, α-smooth muscle actin; CHOP, C/EBP homologous protein; NLRP3, nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain containing 3; TNF-α, tumor necrosis factor α. * <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.</p>
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<p>Effects of HFD and HFD supplemented with fructose or glucose on hepatic ceramides. (<b>A</b>) Levels of C16:0, C16:1, C18:0, C18:1, C20:0, C22:0, C22:1, C24:0, and C24:1 ceramides. (<b>B</b>) Levels of C18:0 and C18:1 ceramides. ND, normal diet; HFD, high-fat diet; HFD + Fru, high-fat diet supplemented with fructose; HFD + Glu, high-fat diet supplemented with glucose. * <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.</p>
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<p>Clinical study results. (<b>A</b>) BMI. (<b>B</b>) ALT. (<b>C</b>) TG, T-chol, HDL-C, and LDL-C levels. (<b>D</b>) Insulin resistance. (<b>E</b>) NASH CRN score. (<b>F</b>) Hepatic ceramide levels. The “mild” group refers to patients with a NASH CRN steatosis score of 0 or 1, whereas the “severe” group includes those with a NASH CRN steatosis score of 2 or 3 or metabolic dysfunction-associated steatohepatitis; ALT, alanine aminotransferase; BMI, body mass index; Cer, ceramide; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment-insulin resistance; LDL-C, low-density lipoprotein cholesterol; NASH CRN, nonalcoholic steatoheaptitis Clinical Research Network; T-chol, total cholesterol; TG, triglyceride. * <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.</p>
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10 pages, 251 KiB  
Article
Effect of Obesity and Metabolic Health Status on Metabolic-Associated Steatotic Liver Disease among Renal Transplant Recipients Using Hepatic Steatosis Index
by I-Hsin Lin, Yi-Ping Yu, Tuyen Van Duong, Shih-Wei Nien, I-Hsin Tseng, Yi-Ming Wu, Yang-Jen Chiang, Chia-Yu Chiang, Chia-Hui Chiu, Ming-Hsu Wang, Nien-Chieh Yang, Ta-Ho Wu and Te-Chih Wong
Nutrients 2024, 16(19), 3344; https://doi.org/10.3390/nu16193344 - 1 Oct 2024
Viewed by 1020
Abstract
Background/Objectives: Obesity and metabolic conditions increase the risk of metabolic-associated steatotic liver disease (MASLD). This study examined the risk of MASLD in 137 renal transplant recipients (RTRs) from a single-center hospital on the basis of their obesity and metabolic health status. Methods: Participants [...] Read more.
Background/Objectives: Obesity and metabolic conditions increase the risk of metabolic-associated steatotic liver disease (MASLD). This study examined the risk of MASLD in 137 renal transplant recipients (RTRs) from a single-center hospital on the basis of their obesity and metabolic health status. Methods: Participants were categorized into four groups: metabolically healthy nonobese (MHNO), metabolically healthy obese (MHO), metabolically abnormal nonobese (MANO), and metabolically abnormal obese (MAO). MASLD was assessed using the hepatic steatosis index (HSI), calculated as 8 × (aspartate aminotransferase/alanine aminotransferase ratio) + body mass index + 2 (if diabetic) + 2 (if woman). The HSI scores were 29.50 ± 4.55, 38.08 ± 5.44, 33.61 ± 5.23, and 39.86 ± 4.13 in the MHNO, MHO, MANO, and MAO groups, respectively (p < 0.05). Results: Overall, 25.55% of the participants (57.14% men) were classified as having MASLD (HSI > 36). A multivariate-adjusted regression analysis revealed significantly higher HSI scores in the MAO group than in the MHNO group. Both MHO and MANO groups also had significantly higher HSI scores. The odds ratios for more severe MASLD were 2.74 (95% CI: 0.88–8.52) for the MANO group and 74.59 (95% CI: 13.29–418.68) for the MAO group compared with the MHNO group. Conclusions: These findings suggest that RTRs with obesity have a higher risk of MASLD, but even those with a normal weight and metabolic abnormalities are at increased risk. Full article
14 pages, 461 KiB  
Article
Improvement of Metabolic-Associated Fatty Liver Disease by Magnetic Resonance Spectroscopy in Morbidly Obese Women Undergoing Roux-en-Y Gastric Bypass, following a Postoperative Mediterranean-like Diet
by Jaime Ruiz-Tovar, Carolina Llavero, Maria Rodriguez-Ortega, Nuria M. De Castro, Maria Cristina Martín-Crespo, Gema Escobar-Aguilar, Ana Martin-Nieto and Gilberto Gonzalez
Nutrients 2024, 16(14), 2280; https://doi.org/10.3390/nu16142280 - 16 Jul 2024
Cited by 2 | Viewed by 1809
Abstract
(1) Background: Bariatric surgery has demonstrated the capacity to improve metabolic-associated fatty liver disease (MAFLD) in patients with morbid obesity. In addition, the Mediterranean diet contains anti-inflammatory, anti-oxidative, and anti-fibrotic components, promoting a beneficial effect on MAFLD. This study aimed to assess the [...] Read more.
(1) Background: Bariatric surgery has demonstrated the capacity to improve metabolic-associated fatty liver disease (MAFLD) in patients with morbid obesity. In addition, the Mediterranean diet contains anti-inflammatory, anti-oxidative, and anti-fibrotic components, promoting a beneficial effect on MAFLD. This study aimed to assess the improvement of MAFLD, specifically liver steatosis, in morbidly obese patients undergoing Roux-en-Y gastric bypass (RYGB) and following a hypocaloric Mediterranean-like diet. (2) Methods: A prospective observational pilot study of 20 patients undergoing RYGB was conducted. The participants underwent a magnetic resonance spectroscopy study 2 weeks before the surgical act and one year postoperatively to assess the percentage of lipid content (PLC). The adherence to the Mediterranean diet was determined by the KIDMED test 1 year after surgery. (3) Results: Mean baseline PLC was 14.2 ± 9.4%, and one year after surgery, it decreased to 4.0 ± 1.8% (p < 0.001). A total of 12 patients (60%) were within the range of moderate adherence to the Mediterranean diet, whereas 8 patients (40%) showed a high adherence. The patients with high adherence to the Mediterranean diet presented significantly lower values of postoperative PLC. (4) Conclusions: Liver steatosis significantly reduces after RYGB. This reduction is further improved when associated with a high adherence to a Mediterranean diet. Full article
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<p>Adherence to the Mediterranean diet according to the KIDMED test.</p>
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13 pages, 1228 KiB  
Article
The Associations between Healthy Eating Patterns and Risk of Metabolic Dysfunction-Associated Steatotic Liver Disease: A Case–Control Study
by Xia Huang, Da Gan, Yahui Fan, Qihui Fu, Cong He, Wenjian Liu, Feng Li, Le Ma, Mingxu Wang and Wei Zhang
Nutrients 2024, 16(12), 1956; https://doi.org/10.3390/nu16121956 - 19 Jun 2024
Cited by 3 | Viewed by 1542
Abstract
Background: Although several epidemiological studies have identified an inverse association between healthy dietary patterns and metabolic dysfunction-associated steatotic liver disease (MASLD)/non-alcoholic fatty liver disease (NAFLD), little is known about the contribution of the food component to MASLD risk and the association between dietary [...] Read more.
Background: Although several epidemiological studies have identified an inverse association between healthy dietary patterns and metabolic dysfunction-associated steatotic liver disease (MASLD)/non-alcoholic fatty liver disease (NAFLD), little is known about the contribution of the food component to MASLD risk and the association between dietary patterns and severity of MASLD. This study aimed to investigate the association between healthy eating patterns and MASLD risk and severity of MASLD. Methods: A case–control study including 228 patients diagnosed with MASLD and 228 controls was conducted. The modified Alternate Healthy Eating Index (AHEI), Dietary Approaches to Stop Hypertension (DASH) score, and Alternative Mediterranean Diet (AMED) score were evaluated based on information collected via a validated food-frequency questionnaire. MASLD was confirmed if participants presented with ultrasound-diagnosed fatty liver diseases along with at least one of five cardiometabolic risk factors and no other discernible cause. The logistic regression models were applied to estimate the odds ratio (OR) and 95% confidence interval (95% CI) of MASLD for dietary scores. Results: Compared with participants in the lowest tertile, those in the highest tertile of AHEI had a 60% reduced risk of MASLD (OR: 0.40; 95% CI: 0.25–0.66). Similar associations were also observed for DASH and AMED, with ORs comparing extreme tertiles of 0.38 (95% CI: 0.22–0.66) and 0.46 (95% CI: 0.28–0.73), respectively. Further Stratified analysis revealed that the inverse associations between AHEI and DASH with MASLD risks were stronger among women than men, and the inverse associations between AMED and MASLD risks were more pronounced among participants with normal weight (OR: 0.22; 95% CI: 0.09–0.49). For components within the dietary score, every one-point increase in vegetable score and whole grain score within the AHEI was associated with an 11% (95% CI: 5–16%) and a 6% (95% CI: 0–12%) lower MASLD risk, respectively. Similar inverse associations with those scores were observed for the DASH and AMED. Conclusion: Greater adherence to healthy eating patterns was associated with reduced risk of MASLD, with vegetables and whole grains predominately contributing to these associations. These findings suggested that healthy eating patterns should be recommended for the prevention of MASLD. Full article
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Figure 1
<p>Restricted cubic spline analyses of associations between three dietary scores and risk of metabolic dysfunction-associated steatotic liver disease. Odds ratios were adjusted for age (continuous), education level (high school and below or college and above), monthly household income (&lt;7000, ≥7000 yuan/capita), marriage (single/divorced/widowed or married/living together), physical activity (&lt;21, ≥21 metabolic equivalents of task-hours/week), smoking (yes or no), and total energy intake (continuous).</p>
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<p>Stratified analyses of associations between three dietary scores and risk of metabolic dysfunction-associated steatotic liver disease (comparing the highest tertile of the dietary score with the lowest tertile). Odds ratios were adjusted for age (continuous), sex (male or female), education level (high school and below or college and above), monthly household income (&lt;7000, ≥7000 yuan/capita), marriage (single/divorced/widowed or married/living together), physical activity (&lt;21, ≥21 metabolic equivalents of task-hours/week), smoking (yes or no), and total energy intake (continuous). OR = odds ratio; CI = confidence interval.</p>
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<p>Associations between each component score within the three dietary scores and risk of metabolic dysfunction-associated steatotic liver disease. Odds ratios were adjusted for age (continuous), education level (high school and below or college and above), monthly household income (&lt;7000, ≥7000 yuan/capita), marriage (single/divorced/widowed or married/living together), physical activity (&lt;21, ≥21 metabolic equivalents of task-hours/week), smoking (yes or no), and total energy intake (continuous). OR = odds ratio; CI = confidence interval.</p>
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