Trevor Lloyd; Mason Poffenbarger; Austin Ricks; Andrew Barlow; Zoey Fishburn, Brigham Young University
Diabetes mellitus reduces and eventually depletes a person’s ability to regulate his or her blood glucose levels due to either pancreatic beta cell death or reduced sensitivity to insulin throughout the body. Preliminary cell death and insulin insensitivity necessitate increased insulin production by the remaining beta cells. This increased demand on the cells eventually leads to the death of additional beta cells perpetuating the cycle and exacerbating the problem. Type II Diabetes (T2D) is characterized by increased levels of circulating Free Fatty Acids (FFA), particularly Palmitate (PA)—the primary fatty acid synthesized by the liver. In order to better understand the degenerative effects of increasing FFA levels on pancreatic beta cells, rat beta cell insulinoma (INS-1) cells were incubated in progressively increasing concentrations of PA (0.15 mM, 0.3 mM, and 0.5 mM). The cells cultured in higher concentrations were step-wise increased from culture in lower PA concentrations to simulate the progression of T2D hyperlipidemia. In order to more fully explore and understand how beta cell functionality changes during progressively higher concentrations of FFA, cells from each PA concentration level along with a corresponding control were stimulated with glucose and the secreted insulin was measured. All cells were measured against a control cell line that has received no treatment, which served as a model for a standard, non-diabetic individual. Glucose stimulation, insulin secretion, and total insulin content were measured to provide insight into how we can best prevent and treat diabetic symptoms and causes.