Cavin-3 is a tumor suppressor protein that inhibits Akt signaling, suppresses Warburg metabolism, promotes apoptosis, and protects against cachexia.

Reduced energy expenditure in obesity may result from reduced sensitivity to sympathetic activation due to inflammation-generated signals in adipose tissue.

LRH-1/NR5A2 responds to ER stress by inducing a novel pathway that is required for stress resolution in mice and can be targeted by LRH-1 agonists.

Physical and functional interactions between HNF4A and TAF4 coordinate HNF4A genomic occupancy with pre-initiation complex formation to activate post-natal hepatocyte gene expression.

The enzyme Lpcat3 plays a unique role in the incorporation of arachidonic acid into membranes, which is required for the production of lipoproteins.

A novel Mendelian disease featuring early-onset hypertension is caused by a recurrent gain of function mutation in CACNA1H, which encodes the voltage-gated calcium channel Cav3.2.

A system genetics approach reveals a unique molecular signature of non-alcoholic fatty liver disease in mice and identifies novel genetic factors affecting hepatic steatosis.

Mouse genetic studies reveal that let-7 performs potent tumor suppressive roles, but at the expense of regeneration and tissue homeostasis in the liver, findings with unanticipated therapeutic implications.

An interaction between the brown fat protein CIDEA and the phospholipid phosphatidic acid is vital for the expansion of intracellular lipid droplets for energy storage.

Metabolic stress-induced activation of the JNK3 protein regulates excitatory transmission onto AgRP neurons to regulate food consumption.