Washington University in Saint Louis

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Clay Semenkovich

URL: http://mednews.wustl.edu/sb/page/normal/181.html

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Jim Dryden
Assoc. Dir. of Broadcast Services
jdryden@wustl.edu
(314) 286-0110

Professor of Medicine and Professor of Cell Biology and Physiology

Expertise: obesity, diabetes, lipid disorders, atheroscilerosis, lipid metaboism

Bio:
Semenkovich
Semenkovich
Semenkovich is known for his research on lipid metabolism, obesity and atherosclerosis.

Education:


News Stories & Tip Sheets:

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Quality of life

Activating protein enhances average lifespan, limits age-related disease in mice (http://mednews.wustl.edu/news/page/normal/10687.html)

Dec. 4, 2007 -- Metabolism researchers at the School of Medicine have found that although it does not extend maximum lifespan in mice, activating a protein in muscle tissue increases average lifespan and prevents some age-related diseases. The researchers believe a similar approach may someday help people avoid age-related problems such as atherosclerosis, diabetes, hypertension and even some cancers.


Volunteers needed

Researchers look to malaria medication to prevent or delay atherosclerosis (http://mednews.wustl.edu/news/page/normal/10525.html)

Nov. 7, 2007 -- Researchers at the School of Medicine are seeking volunteers who are slightly overweight or who have elevated blood pressure. They want to see whether it's possible to reduce the progression of atherosclerosis in healthy people by giving low doses of the malaria drug chloroquine.


Unnerving signals

Interfering with vagal nerve activity in mice prevents diabetes and hypertension (http://mednews.wustl.edu/news/page/normal/8718.html)

Feb. 6, 2007 --
Semenkovich
Semenkovich
Interrupting nerve signals to the liver can prevent diabetes and hypertension in mice, according to scientists at the School of Medicine. The finding is reported in the February issue of the journal Cell Metabolism. A research team led by Clay Semenkovich surgically removed the vagus nerve in mice and found the procedure prevented or reversed the development of insulin resistance and high blood pressure in mice primed to develop these disorders through treatment with glucocorticoids.


Drug for possible diabetes prevention

Common cause of heart disease, diabetes may be treatable with malaria drug (http://mednews.wustl.edu/news/page/normal/8203.html)

Nov. 7, 2006 -- Studies of a rare genetic condition that increases cancer risk have unveiled a potential treatment for metabolic syndrome, a common disorder that afflicts as many as one in every four American adults and puts them at sharply increased risk of type 2 diabetes and clogged arteries.


New targets for treating vascular disease

Bad metabolism in blood vessels linked to high blood pressure, atherosclerosis (http://mednews.wustl.edu/news/page/normal/5348.html)

May 23, 2005 -- An experiment that turned out very differently than expected led scientists at the School of Medicine to the first direct link between inefficient metabolism and atherosclerosis.



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Clips:

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Study suggests new factor contributing to heart disease
St. Louis Post-Dispatch and 35 others

May 26, 2005 -- According to a new WUSTL study published in Nature, faulty metabolism can damage your heart. This new study indicates that bad metabolism could cause blockages in blood vessels, which can lead to heart attacks and strokes. WUSTL cell biologist and physiologist Clay Semenkovich comments.


Need to eat some fat to burn fat
myDNA.com and 9 others

May 10, 2005 -- Working with mice, WUSTL researchers led by cell biology and physiology professor Clay Semenkovich found that where fat comes from determines whether the body can metabolize it effectively. Fat around the belly, thighs or bottom can't be burned efficiently unless "new" fat is eaten in the diet or made in the liver.



Additional Background: Semenkovich's research focuses on how the body breaks down and uses fats called lipids. In particular, he investigates how this process can promote narrowing and hardening of the arteries -- a disease known as atherosclerosis -- in people with diabetes. Using genetically modified mice, Semenkovich has shown that an enzyme called LPL can promote atherosclerosis and affect insulin secretion. In attempt to combat the heart disease, diabetes and obesity that have been shown to accompany a high-fat diet, Semenkovich has created a strain of mice that produce a protein called uncoupling protein-1 in their skeletal muscles. Production of that protein mimics the effects of exercise in the mice. These mice were able to consume high-fat diets and stay healthy and slim, despite lack of exercise. Semenkovich also uses genetically engineered mice to study the role of metabolism in aging and atherosclerosis.
Related Information


Related Links:
•Semenkovich's web page (http://wuphysicians.wustl.edu/physician2.asp?PhysNum=754)
•Department web page (http://wuphysicians.wustl.edu/dept.asp?pageID=1&ID=22)

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