![]() Assistant Professor |
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Research in the laboratory is concerned with the regulation of sympathetic outflow in normal and disease states. Type 2 diabetes is one of the diseases with the greatest risk of developing cardiovascular disease. Accumulated evidence indicates that type 2 diabetes is associated with enhanced sympathetic neural drive. Chronic sympathetic activation increases the risk of cardiovascular complications and subsequent mortality during type 2 diabetes. Our central hypothesis is that enhanced leptin-glutamate signaling in the hypothalamic nuclei contributes to the exaggerated sympatho-excitation in rats with type 2 diabetes The questions are addressed using high fat and low dose streptozotocin-induced type 2 diabetic rats to define the precise mechanisms (leptin-glutamate signaling) and specialized cells (neuron-astrocyte interaction) within the hypothalamus that lead to sympatho-excitation in type 2 diabetes. Furthermore, we also study the effects of leptin through transient receptor potential canonical channels contributing to the exaggerated sympathetic activation in type 2 diabetes. The project is addressed by using whole animal study, electrophysiological study, genetic manipulation, immunohistochemistry, confocal image, neuronal cell culture and molecular biology techniques.
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Recent Publications:
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Erika I. Boesen
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Pamela K. Carmines
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Kurtis G. Cornish
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Lie Gao
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Matthew Kelso
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Shelby Kutty
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Pascale H. Lane
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Yulong Li
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Paras Mishra
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Babu Padanilam
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Kaushik P. Patel
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Iraklis I. Pipinos
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Shyamal K. Roy
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George J. Rozanski
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Steven C. Sansom
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Harold D. Schultz
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Neeru Sharma
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Carol B. Toris
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Saraswathi Viswanathan
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Hanjun Wang
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Hong Zheng
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Matthew C. Zimmerman
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Irving H. Zucker
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