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During sustained cold exposure, lipid fuel is specifically directed towards brown adipose tissue, but not white adipose tissue, via cold-induced regulation of Angiopoietin-like 4 (ANGPTL4).

Obesity leads to increased phosphatidylcholine turnover in adipose tissue macrophages that makes them susceptible to saturated fatty acid-induced inflammation.

Aging is associated with stress-induced senescence of adipose stromal cells, leading to impaired adipogenesis, oxidative stress, mitochondrial dysfunction, and insulin resistance, all being alleviated by metformin treatment of adipose stromal cells.

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

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.

Adipose tissue derived hematopoietic stem cells from diabetic mice transplanted into healthy animals on a normal diet increase inflammation in adipose tissue and trigger the development of a diabetic state in the recipient animals.

Body mass index and adipose distribution have opposing and broad effects on human blood trait variation by Mendelian randomization analysis, helping to clarify the complex interplay between cardiometabolic traits and hematopoiesis at the genetic level.

Mouse and tissue culture studies reveal that adipose DNA methyltransferase 3a mediates insulin resistance, partially through repressing the expression of FGF21.

ADGRA3 signaling promotes adipose thermogenesis via Gs-PKA-CREB, suggesting hesperetin and ADGRA3 overexpression as obesity therapies.

Non-imprinted genes can contribute to parent-of-origin effects on phenotype through interactions with imprinted genes.