Using genetics, it is possible to uncouple higher adiposity from its adverse metabolic effects and show that some obesity-associated conditions may benefit from treating the metabolic effects alone, whilst others may benefit more from weight loss.

Inhibiting triglyceride storage in adipose tissue prevents obesity and improves metabolic health.

Gene regulation by C/EBPβ determines how surplus of dietary fat is stored, which has consequences for metabolic health.

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.

Mice made obese by feeding a high starch diet do not develop insulin resistance like mice made similarly obese by a high fat diet and this is associated with differences in specific bioactive ceramide species in liver and muscle tissue.

A muscle-derived signaling molecule suppresses excessive accumulation of lipids in the Drosophila adipose tissue by activating the Pi3K/Akt/mTOR signaling cascade in the Drosophila hepatocyte-like cells.

An update on the role of lncRNAs in adipogenesis and adipose tissue function, aimed at promoting the identification of new drug targets for obesity and metabolic diseases.

Increased production of ether lipids is required to extend lifespan in response to metformin, phenformin, and multiple, distinct, longevity-promoting manipulations, illuminating the possibility that raising ether lipid levels represents a new therapeutic strategy to support healthy aging.

Circulating high-molecular-weight (cHMW) adiponectin levels increased with age until centenarians, and the contribution of known major factors associated with cHMW adiponectin levels including BMI varied with age, suggesting that its physiological significance also varies with age in the oldest old.