Genetic interaction and biochemical analyses have unveiled the crucial involvement of CTPS in the regulation of adipocyte growth, lipid metabolism, and metabolic adaptation in Drosophila, achieved through activating the PI3K-Akt-SREBP pathway.

Gain- and loss-of-function studies highlight the important role for angiopoietin-2 to maintain adipose tissue health during metabolic challenges.

Identifying xanthohumol and its derivatives as PPARγ anatagonists provides new insight into how natural compounds beneficially treat obesity and metabolic syndrome, and provide new compounds for therapeutic development.

Obesogenic diet intake throughout adolescence impairs different types of memory through overactivation of specific hippocampal efferent pathways and targeting these overactive pathways has therapeutic potential.

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

Maternal obesity mouse model reveal that melatonin deficiency causes the genomic hyper-methylation of oocytes via increasing the expression of DNA methyltransferases.

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.

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.

A subset of myeloid cells expressing CXCR3 is recruited to the hypothalamus and protects against the metabolic abnormalities generated in diet-induced obesity.

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