The size of subcutaneous, but not visceral, fat depots is dependent on the number of embryonic adipocyte progenitors.

PTRF (Cavin-1) mediates metabolism-regulated ribosomal transcription in mature adipocytes, independent of its role in caveolae formation.

Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.

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

The p.Arg707Trp mutation in Mfn2 causes adipose-specific activation of the integrated stress response, which lowers secretion of adipokines.

Disruption of epoxide hydrolysis inducing oxidative stress and cellular senescence is a novel mechanism responsible for lipoatrophic monogenic diabetes.

A novel secondary adipogenesis pathway is defined that is unique to the bone marrow and is activated with age and in states of metabolic stress.

Fat-body-specific loss of actin isoform Act5C disrupts fat body cell growth and fat storage, lipoprotein secretion, and insulin signaling, revealing a non-canonical role for the cortical actin cytoskeleton in nutrient signaling and inter-organelle trafficking.

Fibro-inflammatory progenitors represent a subpopulation of perivascular cells in visceral adipose tissues of mice that promote inflammation and fibrosis.

The dietary vitamin riboflavin provides the chemical backbone to generate essential substrates that support liver glucose metabolism during low-nutrient conditions.