Under insulinopenic conditions, the hormone adiponectin is essential for lipid uptake specifically in subcutaneous white adipose tissue, and is sufficient to ameliorate islet lipotoxicity.

Binding study of native adiponectin existing in serum supported the importance of T-cadherin but not AdipoRs nor calreticulin.

Adiponectin signaling integrates metabolic state information to regulate circadian clock function in hypothalamic appetite regulating centers, food intake rhythms, and body weight.

Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.

A group of cells that can become adipocytes controls the formation of blood vessels in the bone marrow, and also regulates the differentiation of resident mesenchymal progenitor cells.

A newly identified adipose lineage cell population, MALP, regulates marrow vasculature and osteogenesis in bone.

The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.

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

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

Transient hormonal alterations during early critical developmental periods can have a crucial and long-lasting effect on lifespan in mice.