The goal of my laboratory is to pursue a series of studies focused mainly on two mechanisms that we believe are critical to the pathophysiology of cardiovascular disease in patients with Type 2 DM and prediabetes: Vitamin D deficiency and tissue glucocorticoid excess.

Patients with prediabetes and Type 2 DM have a higher prevalence of vitamin D deficiency and hypertension compared to the general population. Animal and human studies have shown that vitamin D improves peripheral insulin action, suppresses the renin-angiotensin system and decreases vascular inflammatory factors; mechanisms responsible for increased blood pressure (BP). However, there is lack of evidence as to whether the increased prevalence of hypertension and atherosclerosis in patients with diabetes or pre-diabetes is truly influenced by vitamin D deficiency. Our laboratory is using multiple animal models, novel molecular biology techniques and clinical trials to assess whether alterations in the expression of genes related to vitamin D metabolism are responsible for the development of these diseases.

Adipose and hepatic glucocorticoid excess in mice resembles metabolic syndrome, a poorly understood condition characterized by insulin resistance, chronic inflammation and cardiovascular disease. We are interested to find the mechanisms by which glucocorticoids induce hypertension and atherosclerosis. In the past, we have demonstrated that a nuclear transcription factor PPAR a (important for lipid metabolism), and hepatic afferent vagal nerve activation are required for glucocorticoid-induced hypertension and diabetes in mice. Now, we are using genetically engineered mice and classical physiology to characterize the interaction between lipid metabolism and glucocorticoid signaling in critical tissues responsible for the development of atherosclerosis.

Identifying these mechanisms may lead to the development of novel therapies for the treatment of diabetes and cardiovascular disease.

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Endocrinology, diabetes, metabolism

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