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Address: 2-200 BSB
Phone: (319) 335-7895
Mentor: Kamal Rahmouni, PhD
Undergraduate Institution: Grinnell College, Grinnell, IA, BA
Year Entered Into Program: 2012
My research is focused on the neurological regulation of obesity and hypertension by the PI3K-mTORC1 signaling pathway in the hypothalamus. Obesity and hypertension affect one in three Americans and are leading causes of morbidity and mortality. Aberrant leptin action and leptin receptor signaling has emerged as an important mechanism for obesity-induced hypertension. Leptin, an adipocyte-derived hormone, is involved in the regulation of energy homeostasis by controlling food intake and energy expenditure. In addition, leptin has been implicated in the control of blood pressure through its action on sympathetic nerve activity. The cardiovascular sympathetic effect of leptin appears to be mediated by neurons located in the arcuate nucleus of the hypothalamus. Our lab has previously shown that hypothalamic mammalian target of rapamycin complex 1 (mTORC1) signaling is involved in the regulation of blood pressure and sympathetic nerve activity and mediates leptin responses. Moreover, the PI3 kinase (PI3K) pathway appears to link the leptin receptor to mTORC1 signaling in hypothalamic neurons. The goal of my work is to elucidate how the PI3K-mTORC1 axis contributes to leptin regulation of physiological processes using genetically modified mouse models with conditional deletion of components of this axis specifically in proopiomelanocortin (POMC) neurons, which are thought to mediate the sympathetic and arterial pressure responses induced by leptin. This will be determined by analyzing several physiological parameters including blood pressure, sympathetic nerve activity, food intake and body weight in mice fed normal chow or a high fat diet (45% kcal), as well as in response to leptin challenge.
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