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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.

Papers
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Journal Article

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2459 more
- 01 Jan 2016 - 
Journal ArticleDOI

Correction of Hypertriglyceridemia and Impaired Fat Tolerance in Lipoprotein Lipase–Deficient Mice by Adenovirus-Mediated Expression of Human Lipoprotein Lipase

Katherine J. D. A. Excoffon, +12 more
- 01 Nov 1997 - 
TL;DR: It is suggested that liver-targeted adenovirus-mediated LPL gene transfer offers an effective means for transient correction of altered lipoprotein metabolism and impaired fat tolerance due to LPL deficiency.
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Relative hypoglycemia and hyperinsulinemia in mice with heterozygous lipoprotein lipase (LPL) deficiency. Islet LPL regulates insulin secretion.

Bess A. Marshall, +8 more
- 24 Sep 1999 - 
TL;DR: The data suggest that islet LPL is a novel regulator of insulin secretion, and suggest that genetically determined levels of LPL play a role in establishing glucose levels in mice.
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Apolipoprotein B mRNA editing. Validation of a sensitive assay and developmental biology of RNA editing in the rat.

June H. Wu, +4 more
- 25 Jul 1990 - 
TL;DR: Quantitation of the ratio of apoB-48 to apo B-100 mRNA at the different time points showed that RNA editing became highly competent prenatally on Day 19 of gestation in the small intestine, but postnatally after birth in the liver.
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Lysosomal dysfunction results in altered energy balance.

Josh C. Woloszynek, +3 more
- 07 Dec 2007 - 
TL;DR: It is shown that adipose storage deficiency and lower leptin levels are common to five different lysosomal storage diseases (LSDs): MPSI, MPSIIIB, M PSVII, Niemann-Pick type A/B, and infantile neuronal ceroid lipofuscinosis.