Accounting for the impact of smoking, obesity, and alcohol on past mortality trends, we project, compared to common practice, longer individual lifespans and more elderly in society for the future.

Maternal obesity and high-fat diet present metabolic, signaling, and epigenetic impediments to pathogen recognition in fetal innate immune cells that result in a state of immune paralysis during gestation and at birth.

Sulforaphane through NRF2-dependent and -independent cellular and molecular pathways alleviates leptin resistance to reverse the diet-induced obesity.

Down-regulation of GAS6 by M1 macrophages resulted in impaired efferocytosis for synovial apoptotic cells, causing synovial hyperplasia and obesity-associated OA development.

The small macrophage-secreted protein RELMα is a sex-specific protein that protects against diet-induced obesity through regulating the macrophage–eosinophil innate immune axis in the adipose tissue.

Epigenomic and transcriptomic analysis reveals that paternal obesity influences sperm histone H3 lysine 4 tri-methylation enrichment and placenta gene expression, which in turn negatively impact its development and function in a manner that may contribute to metabolic disease in offspring.

Clock protein NR1D1 regulates white adipose tissue expansion and development of obesity-related pathology.

Genetic interaction and biochemical analyses have unveiled the crucial involvement of CTPS in the regulation of adipocyte growth, lipid metabolism, and metabolic adaptation in Drosophila, achieved through activating the PI3K-Akt-SREBP pathway.

Maternal obesity mouse model reveal that melatonin deficiency causes the genomic hyper-methylation of oocytes via increasing the expression of DNA methyltransferases.

Significant technical improvement in single-nucleus RNA-seq reveals distinct adipocyte subpopulations that respond differently to obesity, including those undergoing adaptive healthy expansion and others displaying severe dysfunction.