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.

PDZ-RhoGEF controls adipose tissue abundance and whole body metabolism.

Class 1 histone deacetylase (HDAC) inhibitor MS-275 enhances the efficacy of glucagon-like peptide 1 receptor (GLP-1R) therapy for glycemic control and reduction of obesity.

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.

Maternal obesity alters the fetal cardiac and serum lipidome, promoting early fetal cardiac metabolic maturation, with evidence that the female heart lipidome is more responsive to an in utero obesogenic environment.

Sulforaphane through NRF2-dependent and -independent cellular and molecular pathways alleviates leptin resistance to reverse the diet-induced obesity.

LncRNA-Snhg3 regulates lipid metabolism by affecting chromatin accessibility which indicates that lncRNA-mediated epigenetic modification has a crucial role in the pathology of metabolic dysfunction-associated fatty liver disease.

The development of diet-dependent obesity results in the deterioration of calcium homeostasis in pro-opiomelanocortin-expressing neurons and impaired function of the same neurons.

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

Deletion of optic atrophy 1 in brown adipose tissue induces secretion of growth differentiation factor 15 as a batokine to attenuate diet-induced obesity and improve glucose clearance, hepatic steatosis, and thermoregulation in mice by increasing energy expenditure.