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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

The gut microbiota as an environmental factor that regulates fat storage

Fredrik Bäckhed, +8 more
- 02 Nov 2004 - 
TL;DR: In this article, the authors found that conventionalization of adult germ-free C57BL/6 mice with a normal microbiota harvested from the distal intestine (cecum) of conventionally raised animals produces a 60% increase in body fat content and insulin resistance within 14 days despite reduced food intake.
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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Gut Microbiota from Twins Discordant for Obesity Modulate Metabolism in Mice

Vanessa K. Ridaura, +26 more
- 06 Sep 2013 - 
TL;DR: The results reveal that transmissible and modifiable interactions between diet and microbiota influence host biology and that adiposity is transmissible from human to mouse and that it was associated with changes in serum levels of branched-chain amino acids.
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Mechanisms underlying the resistance to diet-induced obesity in germ-free mice

Fredrik Bäckhed, +3 more
- 16 Jan 2007 - 
TL;DR: GF animals are protected from diet-induced obesity by two complementary but independent mechanisms that result in increased fatty acid metabolism: elevated levels of Fiaf, which induces Pgc-1α; and increased AMPK activity.
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PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis.

Teresa C. Leone, +17 more
- 15 Mar 2005 - 
TL;DR: It is demonstrated that PGC-1α is necessary for appropriate adaptation to the metabolic and physiologic stressors of postnatal life.