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Journal of Undergraduate Research

Keywords

B cell adaptation, Nr4a expression, elevated palmitate concentrations, hyperlipidemia

College

Life Sciences

Department

Nutrition, Dietetics, and Food Science

Abstract

Diabetes’ prevalence is increasing at an alarming rate. Normally, insulin-secreting β-cells in the pancreas regulate proper glucose absorption and storage. Both Type 1 and Type 2 diabetes are characterized by decreased functional β-cell mass and insulin production and increased circulating glucose and fatty acid levels, which damage and destroy surviving β-cells over time. Though hyperlipidemia’s short-term effects are well studied, its long-term effects on β-cells remain unclear because it destroys them (1). We developed unique cell lines to mimic Type 2 diabetes’ progression by culturing INS-1 832/13 β-cells in progressively elevated concentrations of palmitate (a saturated fatty acid), which permitted culture and analysis at high concentrations. We have found that β-cell proliferation and expression of key β-cell function and survival genes, especially the transcription factors Nr4a1 and Nr4a3, are significantly downregulated when cells are treated with 0.15 mM, 0.3 mM, and 0.5 mM concentrations of sodium palmitate. We aimed to shed further light on the effects of Nr4a gene knockdown, as caused by gradually worsening hyperlipidemia, and the mechanisms behind those effects, ultimately promoting investigation into methods by which endogenous β-cells could be protected from the harmful hyperlipidemia that accompanies diabetes.

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