University of Minnesota
College of Food, Agricultural and Natural Resource Sciences
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Minnesota Obesity Center

1997 Grant Awards

Neural Regulation of Uncoupling Proteins 1 (UCP1), 2 (UCP2) and 3 (UCP3).

Catherine M. Kotz, Ph.D.
Department of Food Science and Nutrition
University of Minnesota

Leptin and neuropeptide Y (NPY) have differential and opposing effects on UCP1, UCP2 and UCP3. The objective of this project is to determine the independent effects of leptin and NPY on the gene expression of UCP1, UCP2 and UCP3 in adipose tissue (brown and white) and in skeletal muscle. We will examine whether leptin interacts with NPY to influence UCP1, UCP2 and UCP3 gene expression and determine the influence of opioid blockade in the hindbrain on central leptin-induced alterations in gene expression on the 3 UCPs. The effect of dietary restriction on the gene expression of the 3 UCPs will be examined.


The Effect of Insulin on Vascular Regulation in Viscerally Obese Men.

John R. Halliwill, Ph.D.
Department of Anesthesiology
Mayo Clinic, Rochester, MN

This project explores the link between obesity and hypertension. Normally, insulin mediated vasodilation can offset increased sympathetic vasoconstriction. Obesity is associated with increased levels of sympathetic nerve activity, which may lead to the development of hypertension. However, obesity does not always result in hypertension, and the increased levels of sympathetic activity in obese individuals do not correlate with the presence of hypertension. This strongly suggests that factors in addition to heightened sympathetic nerve activity are involved in the pathogenesis of hypertension in obesity. We hypothesize that the development of insulin-resistance exacerbates the hypertensive effects of increased sympathetic nerve activity in viscerally obese men.

The following issues will be addressed:

  1. Compared to lean men, do viscerally obese men have higher levels of sympathetic nerve activity at rest and are the sympathetic nerve activity responses to sympathoexcitatory stimuli augmented?

  2. In viscerally obese men, is the normal relation between sympathetic nerve activity and vascular resistance augmented to favor excessive vasoconstriction?

  3. In viscerally obese men is the normal blunting of sympathetic vasoconstriction by insulin attenuated in the face of insulin resistance?

Recipients of:

2010 Grant Awards
2008 Grant Awards
2006 Grant Awards
2004 Grant Awards
2003 Grant Awards
2002 Grant Awards
2001 Grant Awards
2000 Grant Awards
1999 Grant Awards
1998 Grant Awards
1997 Grant Awards
1996 Grant Awards
1995 Grant Awards


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