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Does Beta-Cell Specific SPTLC2 Deletion Impede Diabetic Onset?

AJAS · 2017 Biomedical and Health Sciences (inferred)

Courtney Smith · Brigham Young University, Bellevue, NE

Overview

Abstract More than 68.8% of adults are considered to be overweight or obese, with more than 9% of Americans being diabetic (and the majority of these suffering from T2D). Metabolic diseases, such as obesity and diabetes continue to rise in the United States. Prolonged high fat diets result in low-grade inflammation, promoting insulin resistance. Both, T1D and T2D result in loss of b-Cell mass- impeding insulin secretion and normoglycemia. Protecting b-Cells from the cell death observed during T2D could potentially be used as a cure. Our collaborators have shown that Serine Palmitoyltransferase Long Chain Base Subunit 2 (SPTLC2), an enzyme essential in sphingolipids biosynthesis has increased expression in the b-Cells of obese diabetic mice with b-Cell failure. Therefore, we hypothesize that loss of SPTLC2 in the b-Cell will result in increased b-Cell maintenance and delayed diabetic onset in an obesity induced model of T2D. This project will define the role of SPTLC2 in diabetes and its ability to protect the b-Cells from loss in obesity induced T2D.

Competition history

  • AJAS 2017 Category not listed

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Source: AAAS Annual Meeting (Confex) / American Junior Academy of Science

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