Stephen
Previs, PhD
Assistant
Professor
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office:
2109 Adelbert Road
BRB 921
LAB:
2109 Adelbert Road
BRB 901
phone: 216.368-6533
fax: 216.368-6560
email: sxp29@case.edu
mailing address:
Department of Nutrition
Case Western Reserve University
School of Medicine • W-G48
10900 Euclid Avenue
Cleveland OH 44106-4954
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Background
Steve received his Ph.D. in Nutritional
Biochemistry from CWRU (1997). Under the guidance of Dr. Henri Brunengraber,
his thesis focused on evaluating the use of stable isotope tracer
methods for estimating the contribution of gluconeogenesis to glucose
production. He then went to Yale University (1997-1999) as a postdoctoral
fellow under the direction of Dr. Gerald Shulman. While at Yale
he used isotope tracers to characterize the metabolism of various
genetic knockout models of insulin resistance/Type II diabetes.
After two years at Yale he returned to CWRU (1999-2000) as a postdoctoral
fellow under the guidance of Dr. Bernard Landau. He began to focus
his efforts on the study of protein metabolism. He joined the Nutrition
faculty as Assistant Professor in July 2000. During the course of
his research Steve Previs has established many national and international
collaborations.
RESEARCH
INTERESTS
My research is focused on understanding the integration
of carbohydrate, fat and protein metabolism. I am studying the relationship
between obesity and diabetes. Weight management can reduce and/or abolish
the risk of developing diabetes and related complications. My research
has particular importance in devising treatment strategies of overweight/obese
children. For example, since children need to maintain positive energy
balance for normal development therapies must reduce body fat but not
alter protein metabolism.
I am evaluating the role of dietary vs genetic factors
in the development of and reversal of obesity. For example, dietary
models represent cases where insulin resistance/diabetes develops secondary
to weight gain/obesity. On the contrary, genetically engineered mice
represent models of primary insulin resistance/diabetes, i.e. a known
alteration in intracellular signaling exits and can result in weight
gain/obesity presumably independent of diet. Contrasting these models
should provide an understanding of how weight is gained during various
conditions. Once one has a better understanding of how weight is gained
one can target therapies to reverse specific aberrant changes.
I primarily use mass spectrometry and stable isotopes
to estimate biochemical flux. The combination of these techniques allows
me to investigate metabolism in vivo. Although most of my research is
conducted at CWRU I have many national and international collaborations.
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