Aim 1: Confirm the role of IP6K1 in -oxidation/energy expenditure and determine the mechanism. Mouse embryonic fibroblasts (MEFs), isolated from K1-KO mice s...
... middle of paper ...
...ation of inducible IP6K1 depleted 3T3L1 and mouse BAT cell lines; and 4) generation of WAT and BAT cell lines from K1-KO and atK1-KO mice which could be used as cellular anti-obesity models.
The model of the current proposal is outlined in Fig. 1. Aim 1: IP6K1 and AMPK are differentially regulated by cellular energy status. Under normal energy supply, IP6K1 suppresses AMPK. Conversely, energy stress mediated IP6K1 inhibition activates AMPK which regulates ACC and PGC1 dependent -oxidation and thermogenesis. Aim 2: we propose that in adipocytes, IP6K1 binding stabilizes the lipolytic regulator PLIN1 which inhibits basal lipolysis. Starvation activates PKA by -AR stimulation. PKA phosphorylation of IP6K1 disrupts IP6K1-PLIN1 binding which stimulates lipolysis. Aim 3: adipogenic signals induce IP6K1 that promote lipid accumulation and alters adipokine secretion.
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