Projects

Research in the Islet Regeneration Lab focuses on understanding how gene-environment interaction affects the regulation of pancreatic beta cell function, survival and regeneration. Dr. Matveyenko's team is also discovering how circadian clock genes and the circadian system regulate beta cell function and regeneration.

Circadian disruption in obesity, metabolic syndrome and diabetes

Conditions associated with circadian disruption, such as shift work and sleep loss, are increasingly common and increase the susceptibility for the development of obesity, metabolic syndrome and diabetes. Mechanisms responsible for these associations remain unknown. The work in Dr. Matveyenko's Islet Regeneration Lab is focused on elucidating physiological and molecular links driving the association between circadian disruption and loss of glycemic control, with particular focus on the regulation of beta cell function and survival.

Circadian clock genes in the regulation of beta cell function, survival, regeneration and maturation

Intracellular circadian clocks (clock genes) are a highly conserved set of core genes, which exert circadian control over numerous essential cellular functions such as metabolism, proliferation, survival and mitochondrial function. Dr. Matveyenko's research group is exploring molecular mechanisms by which clock genes regulate cellular function, regeneration and maturation with a focus on pancreatic β-cells. Therapeutic regulation of β-cell clock gene expression potentially presents a novel therapeutic approach to combat β-cell pathology in type 2 diabetes.

Type 2 diabetes-associated genetic loci in pathophysiology of beta cell failure

Recent genome-wide association studies have identified numerous genetic loci associated with the development of type 2 diabetes. However, the molecular underpinnings of the described associations remain largely unknown. In collaboration with Adrian Vella, M.D., Dr. Matveyenko's Islet Regeneration Lab is studying how genetic variations in the TCF7L2 and MTNR1B loci affect islet cell morphology, turnover and cellular physiology.

Elucidation of mechanisms underlying the induction of pancreatic cancer-induced diabetes mellitus

Pancreatic cancer is a devastating disease and is the fourth leading cause of cancer-related deaths in the United States. The majority of people with pancreatic cancer also exhibit hyperglycemia that often occurs a few years prior to the cancer diagnosis. The mechanisms driving the development of cancer-induced hyperglycemia are unknown and may provide important insights into pancreatic cancer development and progression. In collaboration with Suresh T. Chari, M.D., Dr. Matveyenko's lab is studying the molecular mechanisms that mediate the induction of hyperglycemia in pancreatic cancer, specifically focusing on the cancer-related effects on insulin-producing beta cells.