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Abstract
By regulating Akt membrane compartmentalization, ClipR-59 modulates adipocyte glucose transport. To elucidate the role of ClipR-59 in the regulation of whole body glucose homeostasis, we have generated adipose tissue specific transgenic mice and examined how forcing expression of ClipR-59 in adipose tissue affects body glucose homeostasis. We found that ClipR-59 adipose transgenic mice showed lower blood glucose level with increased glucose tolerance and enhanced insulin sensitivity. Moreover, ClipR-59 adipose transgenic mice were lean with reduced fat mass and against diet induced obesity. Finally, we examined the potential impact of ClipR-59 on adipose endocrine function and found that ClipR-59 expression enhanced adiponectin secretion in both 3T3-L1 adipocytes and adipose tissue, accompanied with increased circulating adiponectin and enhanced AMPKα phosphorylation at Thr172 in adipose tissue and skeletal muscle. Overall, these studies demonstrate that ClipR-59 is likely an important regulator of body glucose homeostasis and adipocyte function.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Funding
This work was supported by NIH grant RO1 DK084319