Diabetes, Pancreatic beta cell growth and development, Pancreatic beta cells are the sole source of insulin, the hormone required for proper use of glucose. Any defect in production or utilization of insulin result in diabetes.
Our lab is interested in understanding the molecular mechanisms that regulate beta cell mass and function, using pregnancy as the model. Using rodent models, we have found that intact prolactin receptor signaling is required for normal glucose homeostasis and beta cell mass expansion during pregnancy. In the absence of prolactin receptor signaling, the pregnant mice developed gestational diabetes, and the female offsprings born to diabetic mothers are also at increased risk of developing gestational diabetes themselves. We also found evidence of beta cell neogenesis in rodent pregnancy, using lineage tracing techniques.
Our current research focus is on 1) identifying novel signalling pathways required for the increase in β-cell mass and function during pregnancy, and 2) testing whether pregnancy hormones can improve glucose homeostasis in animal models of type 1 and type 2 diabetes.
We use transgenic mice and cell lines as our model systems, using molecular biology, biochemistry, and in vivo physiologic testing techniques to address these questions.
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