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Clay F. Semenkovich
Researcher at Washington University in St. Louis
Publications - 200
Citations - 33711
Clay F. Semenkovich is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Insulin resistance & Fatty acid synthase. The author has an hindex of 70, co-authored 193 publications receiving 30175 citations. Previous affiliations of Clay F. Semenkovich include Rush University Medical Center & Baylor College of Medicine.
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Journal ArticleDOI
Brain fatty acid synthase activates PPARα to maintain energy homeostasis
Manu V. Chakravarthy,Yimin Zhu,Miguel López,Li Yin,David F. Wozniak,Trey Coleman,Zhiyuan Hu,Michael J. Wolfgang,Antonio Vidal-Puig,M. Daniel Lane,Clay F. Semenkovich +10 more
TL;DR: It is reported that the conditional genetic inactivation of FAS in pancreatic β cells and hypothalamus produced lean, hypophagic mice with increased physical activity and impaired hypothalamic PPARα signaling, suggesting a critical role for brain FAS for the regulation of not only feeding, but also physical activity.
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Lipoprotein lipase and hepatic lipase mRNA tissue specific expression, developmental regulation, and evolution.
TL;DR: Comparison of sequences from mouse, human, bovine, and guinea pig cDNAs indicated that the rates of evolution of mouse,human, andbovine LPL are quite low, but guinea Pig LPL has evolved several times faster than the others.
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Exercise induces human lipoprotein lipase gene expression in skeletal muscle but not adipose tissue
TL;DR: The existence of an exercise stimulus intrinsic to skeletal muscle, which raises LPL activity in part by pretranslational mechanisms, is suggested, a process that contributes to the improvement in circulating lipids seen with physical activity.
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Induction of human skeletal muscle lipoprotein lipase gene expression by short-term exercise is transient.
TL;DR: The time course of the LPL response to both short-term and acute exercise was examined and circulating levels of putative regulators of muscle LPL were measured to suggest induction of LPL gene expression may result from dynamic changes in serum catecholamines, plasma insulin, or events intrinsic to muscle contraction itself.
Journal ArticleDOI
Insulin Resistance and Atherosclerosis
TL;DR: Current thinking that is shaping molecular understanding of insulin resistance and atherosclerosis is addressed, and promising drugs such as the thiazolidinediones have come under scrutiny for possible deleterious CV effects.