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Matthew Lloyd

Research Assistant

My project aims to improve our understanding of how hyperglycaemia impairs pancreatic beta-cell function. Using both an insulin-secreting cell line and whole islets, I am exploring the metabolic changes and molecular mechanisms underlying the decline in insulin biosynthesis that occurs in chronic hyperglycaemia. I am also investigating the causes and consequences of glycogen storage in diabetic beta-cells. As pancreatic islets do not normally store glycogen, the effects of glycogen accumulation on beta-cell function are uncertain. My work will contribute to a mechanistic understanding of why beta cells eventually fail in type 2 diabetes.