Presenter: Chad Mourino
Authors: Chad Mourino
Faculty Advisor: Jeffery Tessem
Institution: Brigham Young University
Over 10% of the US population has Type 2 Diabetes (T2D), which is a disease of the insulin-secreting pancreatic β-cell within the islets of Langerhans. β-cells secrete insulin in response to elevated blood glucose to induce certain cell types to take up and utilize glucose. T2D results in elevated blood glucose levels due to insulin resistance and decreased glucose uptake in skeletal muscle and adipose tissue. This can lead to β-cell exhaustion and an eventual decrease in β-cell mass. Some complications of prolonged high blood glucose levels include neuropathy, damaged blood vessels, and poor wound healing. Although T2D is commonly associated with dysfunctional β-cells, dysfunctional α-cells within islets also negatively influence blood glucose levels. Dysfunctional α-cells lead to high levels of the hormone glucagon, that stimulates increased glucose production and release to circulation, further elevating blood glucose levels. Both β- and α-cells have very similar developmental pathways and mechanisms of hormone secretion. Defining the molecular pathways that result in dysfunctional β- and α-cells are essential for designing cures for diabetes. Certain dietary compounds have beneficial effects on β-cells, including some from cocoa. We previously showed that cocoa flavonoids (such as epicatechin) improve mitochondrial respiration and glucose-stimulated insulin secretion in β-cells. Increased insulin secretion, early in T2D onset, is sufficient to maintain blood glucose levels. A decrease in α-cell glucagon secretion in the T2D condition may also contribute to blood glucose level maintenance. Here we show the effects of a cocoa flavonoid on α-cell mitochondrial respiration and glucose-regulated glucagon secretion.