Jefferson C. Frisbee, Ph.D.
	Associate Professor of Physiology and Pharmacology Graduate Training: University of Guelph Fellowship: University of Washington & Medical College of Wisconsin
	Office: 3002-HSN Lab: 3145-HSN PO Box 9105 Morgantown, WV 26506	Email: jfrisbee@hsc.wvu.edu Phone: 304-293-6527 Fax: 304-293-5513

Research Interests:

A developing characteristic of the metabolic syndrome, defined as the combined presentation of obesity, insulin resistance/type II diabetes mellitus, dyslipidemia and hypertension, is a progressive inability to match blood flow to working tissues with metabolic demand arising from those tissues, such that an evolving ischemic condition develops. While this syndrome presently afflicts more than 47 million Americans (American Heart Association), defining specific causes underlying this perfusion/demand mismatch has been challenging, as previous studies in human subjects have determined that alterations to vascular reactivity, a progressive structural narrowing of individual vessels, and a developing reduction in the density of microvessels within skeletal muscle can all occur during the metabolic syndrome in afflicted individuals. Each of these conditions has the potential to elevate vascular resistance and compromise the ability of skeletal muscle to resist fatigue through impairments in the processes of mass transport and exchange.

Our research program is targeted at understanding alterations to microvascular structure and function during the development of the metabolic syndrome. While individual projects examine alterations to microvascular reactivity to physiological and pharmacological stimuli, additional efforts are directed at understanding modifications to microvascular structure (at both the individual vessel and whole network levels of resolution) which develop with the metabolic syndrome. However, the underlying purpose of these projects is the integrative understanding of how alterations to both structure and function of the microcirculation combine to impact perfusion to the individual organ or tissue in question in animals afflicted with the full metabolic syndrome or with individual components of it.

While the predominant research thrust of the laboratory employs the Zucker rat model of the metabolic syndrome (one brought on by hyperphagia), other avenues of investigation are employing models of the constituent elements of the metabolic syndrome (i.e., hypertension, insulin resistance, dyslipidemia). Further, while much of our previous investigation has focused on alterations to microvascular structure/function and perfusion within the skeletal muscle circulation, evolving projects focus on cerebrovascular behavior during the metabolic syndrome and on the regulation of pulmonary microvascular structure and function as well.

Selected Publications:

1. Goodwill AG, Stapleton PA, James ME, d'Audiffret AC, Frisbee JC. Increased arachidonic acid-induced thromboxane generation impairs skeletal muscle arteriolar dilation with genetic dyslipidemia. Microcirculation. 2008 [Epub ahead of print]
2. Goodwill AG, James ME, Frisbee JC. Increased vascular thromboxane generation impairs dilation of skeletal muscle arterioles of obese Zucker rats with reduced oxygen tension. Am J Physiol Heart Circ Physiol. 2008 [Epub ahead of print]
3. Peterson JM, Bryner RW, Frisbee JC, Alway SE. Effects of Exercise and Obesity on UCP3 Content in Rat Hindlimb Muscles. Med Sci Sports Exerc. 2008 [Epub ahead of print]
4. Stapleton PA, James ME, Goodwill AG, Frisbee JC. Obesity and vascular dysfunction. Pathophysiology. 2008, 15(2):79-89.
5. Samora JB, Frisbee JC, Boegehold MA. Hydrogen peroxide emerges as a regulator of tone in skeletal muscle arterioles during juvenile growth. Microcirculation. 2008;15(2):151-61.
6. Stapleton PA, Goodwill AG, James ME, Frisbee JC. Altered mechanisms of endothelium-dependent dilation in skeletal muscle arterioles with genetic hypercholesterolemia. Am J Physiol Regul Integr Comp Physiol. 2007;293(3):R1110-9.
7. Frisbee JC. Obesity, insulin resistance, and microvessel density. Microcirculation. 2007;14(4-5):289-98.
8. Frisbee JC, Samora JB, Basile DP. Angiostatin does not contribute to skeletal muscle microvascular rarefaction with low nitric oxide bioavailability. Microcirculation. 2007;14(2):145-53.

Lab Personnel: Milinda James - Research Assistant II Adam Goodwill - Ph.D. Student Phoebe Stapleton - Ph.D. Student
	Front: Phoebe Stapleton, Milinda James Back: Alexandre d'Audiffret, M.D., Jefferson Frisbee, Ph.D., Adam Goodwill