J
Jean E. Schaffer
Researcher at Washington University in St. Louis
Publications - 113
Citations - 13271
Jean E. Schaffer is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Lipotoxicity & Fatty acid. The author has an hindex of 51, co-authored 110 publications receiving 11923 citations. Previous affiliations of Jean E. Schaffer include Massachusetts Institute of Technology & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
Triglyceride accumulation protects against fatty acid-induced lipotoxicity
Laura L. Listenberger,Xianlin Han,Sarah Lewis,Sylvaine Cases,Robert V. Farese,Daniel S. Ory,Jean E. Schaffer +6 more
TL;DR: This work demonstrates in cultured cells that the relative toxicity of two common dietary long chain fatty acids is related to channeling of these lipids to distinct cellular metabolic fates, and supports a model of cellular lipid metabolism in which unsaturated fatty acids serve a protective function against lipotoxicity though promotion of triglyceride accumulation.
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Expression cloning and characterization of a novel adipocyte long chain fatty acid transport protein.
TL;DR: Immunocytochemistry and subcellular fractionation of 3T3-L1 adipocytes show that FATP is localized to the plasma membrane, and it is proposed thatfatP is a plasma membrane transporter for LCFAs.
Journal ArticleDOI
Lipotoxicity: when tissues overeat.
TL;DR: This review will provide the reader with an update on the understanding of the adverse effects of fatty acid accumulation in non-adipose tissues, a phenomenon known as lipotoxicity.
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A novel mouse model of lipotoxic cardiomyopathy.
Hsiu-Chiang Chiu,Attila Kovacs,David A. Ford,Fong-Fu Hsu,Ricardo Garcia,Pilar Herrero,Jeffrey E. Saffitz,Jean E. Schaffer +7 more
TL;DR: It is demonstrated that fatty acid uptake/utilization mismatch in the heart leads to accumulation of lipid species toxic to cardiac myocytes, and a novel mouse model of metabolic cardiomyopathy is established to provide insight into the role of perturbations in myocardial lipid metabolism in the pathogenesis of inherited and acquired forms of heart failure.
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Palmitate-induced apoptosis can occur through a ceramide-independent pathway.
TL;DR: The data suggest that palmitate-induced apoptosis occurs through the generation of reactive oxygen species, independent of ceramide synthesis, is important for the lipotoxic response and may contribute to the pathogenesis of diseases involving intracellular lipid accumulation.