Anti-Drug Leads to Increased Insulin Sensitivity in Obese CD1 Mice

Primary Author

Juan Estevez

Additional Author(s)

U-Ter Aondo Jia, Yessenia Perez

Faculty Mentor

Dr. Eunhee Chung

Additional Mentor(s)

Dr. Francis Yoshimoto

Abstract

Obesity is a prevalent disease affecting 4 in 10 Americans in which the intake of fatty foods is a main contributor. The CYP8B1 gene is associated with obesity as it plays a key role in bile acid production and downstream is vital to insulin sensitivity. Previous studies have shown success in the knockout treatment in mice of the sterol 12a-hydroxylase gene (CYP8B1) and its correlation to increased secretion of GLP-1 and increased free fatty acid concentration in the ileal lumen that leads to decrease absorption of fats and enhanced glucose tolerance. Instead of utilizing knockout mice, this study utilizes diet intervention and drug intervention. A novel synthesized anti-drug is used to inhibit the CYP8B1 gene, with the aim of having the effect of lower body weight and increased glucose metabolism. In order to characterize the data in both qualitative and quantitative ways, different procedures such as glucose tolerance test (GTT), insulin tolerance test (ITT), western blot, and analysis of variance were used. As a successful outcome of this study, the mice that gained weight and became diabetic will have a reverse effect and will have a decrease in weight as well as lower blood glucose levels. This innovative way of weight loss and diabetes control can be a new therapy in the future that may lead to promising results in human subjects and in the pharmaceutical market.

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