The Need to Treat Obsesity in the United States Essay

The Need to Treat Obsesity in the United States Essay

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The prevalence of obesity-related comorbidities such as type-2 diabetes and heart diseases in the US emphasizes the need for concerted efforts to prevent and treat obesity1-3. A decrease in 5% of body weight significantly reduces cardiovascular risk in humans4 which proves the urgency of weight management. A combination of drug and lifestyle intervention is ideal for obesity management5-8. Unfortunately, the current anti-obesity medications that inhibit food intake or absorption are partly effective9,10. Thus, an alternate approach is to target energy metabolism11-19 due to the fact that obesity results when energy storage in the adipose tissue exceeds its expenditure20. However, due to the complexity of adipose tissue21, the fundamental understanding of the mechanism and regulation of its metabolism is still lacking22,23. Using a knockout mouse model, we previously reported that IP6K1, an enzyme in the inositol phosphate pathway24, is a novel regulator of energy metabolism25. IP6K1 knockout (K1-KO) mice are protected against age and high fat diet induced weight gain and insulin resistance, despite unaltered food intake25. The objective of the current proposal is to determine the mechanisms by which IP6K1 promotes lipid accumulation in adipose tissue. Our central hypothesis is that IP6K1 is a major regulator of adipose tissue energy metabolism. To test this, we propose to determine role of IP6K1 in 1) oxidation and energy expenditure; 2) lipolysis and 3) adipogenesis. Furthermore, we propose to determine the underlying mechanisms by which IP6K1 regulates these processes.

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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