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Megan Capozzi received her BA in Neuroscience at Vanderbilt University in 2011. She completed her PhD in Molecular Physiology and Biophysics in 2016 from Vanderbilt University, where she studied inflammation in diabetic retinopathy with Dr. John Penn. She then completed a postdoctoral fellowship with Dr. Jonathan Campbell at Duke University in 2023, where she studied the role of islet alpha to beta cell communication in glucose metabolism. This research showed that glucagon from the alpha cell potentiated insulin secretion, suggesting a more complex role for glucagon in postprandial metabolism. Dr. Capozzi was recruited to the Department of Medicine and appointed to Assistant Professor in Fall of 2023.

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Research Interests

Diabetes is a disease characterized by abnormal nutrient metabolism that can be attributed in part to hormonal dysregulation. Impaired insulin secretion or insulin sensitivity coupled with elevated glucagon secretion has been thought to drive diabetic hyperglycemia. Glucagon receptor agonism and antagonism have both been pursued as a treatment strategy for diabetes; blockade of glucagon activity prevents glucose output but activation of glucagon receptor stimulates energy expenditure. Thus, a better understanding of glucagon metabolism is needed.

Our lab is interested in the effect of glucagon and insulin co-secretion after meal ingestion, as mixed-nutrient feeding stimulates secretion of both hormones from the islet. Interestingly, glucagon and insulin appear to work together to initiate unique signaling in the liver, but the effects of their crosstalk on glucose metabolism remains incompletely defined. Hepatic glycogen storage is dysregulated in diabetes and steatotic liver disease, so understanding how altered hormone secretion relates to glycogen storage is a primary focus of the lab. Ultimately, we want to use this understanding to identify treatment strategies that optimize energy metabolism in the liver.

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How can this research help people with diabetes?

Our goal is to understand the normal physiology of nutrient use and storage following a meal. We will use this information to inform how this system may be malfunctioning in metabolic diseases such as diabetes and steatotic liver disease. With this knowledge, we hope to identify new targets for treatment of metabolic diseases.