Targeted activation of Hedgehog signalling via Gli2 facilitated the reduction of high-fat-diet-induced obesity and improvement of whole-body glucose tolerance and insulin sensitivity in adult mice.

The preoptic area (POA) regulates distinct metabolic adaptations, via leptin-dependent (fasting-induced hypometabolism and high-fat-diet-induced hypermetabolism), or leptin-independent mechanisms (temperature induced metabolic changes) and thus significantly contributes to body weight homeostasis.

Endogenous synthesis of fatty acids by oligodendrocytes is essential for development and repair in the central nervous system.

In depth characterization of gene expression in the mouse hypothalamus will facilitate understanding of the molecular pathways that affect metabolic traits and discovers new genes associated with these pathways.

NOVA pre-mRNA spacing factors suppress adipose tissue energy expenditure.

B cell lymphoma 6 (BCL6) represses fasting gene expression by opposing peroxisome proliferator-activated receptor alpha (PPARa) activity at enhancers, and its ablation protects against steatosis by enhancing fatty acid catabolism.

The major protein disulfide isomerase family member, PDIA1, is essential in beta cells of mice fed a high-fat diet to maintain glucose homeostasis, proinsulin maturation and organelle integrity.

Stimulation of endothelial glucose metabolism and vascular growth by genetic depletion of endothelial Foxo1 improves the whole-body response to a high-fat diet, by preserving adipose tissue functions and glucose homeostasis.

Great care is needed when interpreting claims about the genetic basis of human variation based on data from genome-wide association studies.

A subgroup of the neurons that control muscles becomes less excitable shortly before the symptoms of ALS develop.