Insulinergic neuromodulation of hedonic food processing predicts future weight management and improves with weight loss in older overweight dieters.

Profiling the adipocyte secretome reveals LRG1 as a novel adipokine that promotes insulin sensitivity and modulates inflammation triggered by release of cytochrome c from dead/dying cells, describing a new pathway at the intersection of obesity and its systemic sequelae.

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 truncated, non-signaling insulin receptor regulates insulin sensitivity in the nematode C. elegans by sequestering insulin peptides and preventing their interaction with full length receptors.

Genetic inactivation of the transcription factor, Zfp423, in visceral white adipocyte precursors leads to the formation of thermogenic adipocytes in visceral fat depots and improves insulin sensitivity in obese mice.

Senescent cells contribute to age-related fat dysfunction and can directly impair healthy fat progenitor function, in part, via the secretion of activin A.

Lower mitochondrial coenzyme Q was a consistent feature across multiple in vitro and in vivo models of insulin resistance and was sufficient to cause insulin resistance through increased mitochondrial oxidants.

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.

A proteomics screening in mouse adipose tissue shows that loss of adipose Hexokinase 2 is a mechanism of obesity-induced insulin insensitivity.

The centipede peptide toxin SpTx1 blocks the pore of ATP-sensitive potassium channels in pancreatic β cells to markedly enhance insulin secretion and mitigate hyperglycemia in diabetic mice insensitive to the anti-diabetic sulfonylurea glibenclamide.