Rachael M. Easton

TL;DR: The function of Akt3 is addressed, which is not required for the maintenance of normal carbohydrate metabolism but is essential for the attainment of normal organ size, in contrast to Akt1− / − mice, which display a proportional decrease in the sizes of all organs,Akt3 −/− mice present a selective 20% decrease in brain size.

TL;DR: It is shown that the genetic loss of Akt1, but not Akt2, in mice results in defective ischemia and VEGF-induced angiogenesis as well as severe peripheral vascular disease.

TL;DR: It is shown that Akt2 is required for hepatic lipid accumulation in obese, insulin-resistant states induced by either leptin deficiency or high-fat diet feeding, and is a requisite component of the insulin-dependent regulation of lipid metabolism during insulin resistance.

TL;DR: A noncanonical Akt-independent, phosphoinositide-3 kinase (PI3K)-dependent pathway that regulates adipocyte lipolysis using restricted subcellular signaling is described that selectively alters the PKA phosphorylation of its major lipid droplet-associated substrate, perilipin.

TL;DR: Genetic loss of function experiments are utilized to show that constitutive activation of neither FoxA2 nor FoxO1 can account for the protection from steatosis afforded by deletion of Akt2 in liver, and insulin signaling throughAkt2 promotes anabolic lipid metabolism independent of Foxa2 or Fox O1 and through pathways additional to the mTORC1-dependent activation of SREBP1c.