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Mouse obesity model: Mito-OB™ mouse

Detailed Technology Description
Dr. Mishra’s mouse model;  Mito-OB ® has a specific alteration of prohibitin gene expression in white adipose tissue.  Animals become obese and insulin resistant in a manner analogous to human obesity, diabetes and metabolic syndrome.  Existing mouse obesity molecules are based on appetite dysregulation by the leptin system or un-defined characteristics of obesity-selected strains.   For this reason the results of pharmacology and other therapeutic experiments on currently-available mouse obesity models may be  misleading or even useless.
*Abstract

Mito-OB ® mouse model elucidates the regulation of adipose tissue homeostasis and its impact on metabolic regulation. This transgenic mouse model, Mito-Ob®, over-expresses prohibitin (PHB) in adipocytes. Mito-Ob® mice developed obesity due to up-regulation of mitochondrial biogenesis in adipocytes. Mito-Ob®  female mice developed more visceral fat than male mice. MitoOb® male mice had impaired glucose homeostasis, compromised brown adipose tissue structure, and high insulin and low adiponectin levels.  Mechanistically, the inventors found that PHB overexpression enhances the cross talk between the mitochondria and the nucleus as well as it facilitates mitochondrial biogenesis. The data suggest a critical role of PHB and adipocyte mitochondria in adipose tissue homeostasis and reveal sex differences in the effect of PHB-induced adipocyte mitochondrial remodeling on whole-body metabolism. Targeting adipocyte mitochondria may provide new therapeutic opportunities for the treatment of obesity, a major risk factor for type 2 diabetes.  The transgenic mice provide a heretofore unavailable animal model (with a well defined metabolic defect) of obesity, insulin resistance and metabolic syndrome. In contrast, existing mouse obesity molecules are based on appetite dysregulation by the leptin system or un-defined characteristics of obesity-selected strains.

*Inquiry
Odd Bres,Ph.D.TechnologyManagerPh:+1(204)474.9407Email: odd.bres@umanitoba.ca
Country/Region
USA

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