S
Sheng-Li Zhou
Researcher at Icahn School of Medicine at Mount Sinai
Publications - 21
Citations - 908
Sheng-Li Zhou is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Fatty acid & Membrane transport. The author has an hindex of 14, co-authored 21 publications receiving 878 citations. Previous affiliations of Sheng-Li Zhou include City University of New York.
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Journal ArticleDOI
Uptake of Long Chain Free Fatty Acids Is Selectively Up-regulated in Adipocytes of Zucker Rats with Genetic Obesity and Non-insulin-dependent Diabetes Mellitus
TL;DR: These studies indicate 1) that regulation of fatty acid uptake is tissue-specific and 2) that up-regulation of adipocyte fatty acids uptake is an early event in Zucker fa/fa rats, independent of the role of any particular fatty acid transporter.
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Comparison of plasma membrane FABP and mitochondrial isoform of aspartate aminotransferase from rat liver
TL;DR: Comparison of the chemical and immunological properties of rat liver m-AspAT with those ofRat liver FABPpm isolated by two procedures revealed no differences with respect to NH2-terminal amino acid sequence, amino acid composition, peptides from tryptic digests, AspAT enzymatic activity, and isoelectric point.
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Adipocyte differentiation of 3T3-L1 cells involves augmented expression of a 43-kDa plasma membrane fatty acid-binding protein.
TL;DR: In 8-day adipocytes saturable oleate uptake was inhibited by up to 55% by antibodies against rat liver FABPPM; these antibodies had no effect on uptake of 2-deoxyglucose or the medium chain fatty acid octanoate, and these studies support the hypothesis that FABpPM is a component of a saturable transport mechanism for long chain fatty acids.
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Ethanol up-regulates fatty acid uptake and plasma membrane expression and export of mitochondrial aspartate aminotransferase in HepG2 cells
TL;DR: The data suggest that the increased plasma mAspAT observed in alcoholics may reflect pharmacologic upregulation of m aspartate aminotransferase mRNA and of mAsPAT synthesis by ethanol; and increased m aspAT‐mediated fatty acid uptake may contribute to alcoholic fatty liver.
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Insulin- and leptin-regulated fatty acid uptake plays a key causal role in hepatic steatosis in mice with intact leptin signaling but not in ob/ob or db/db mice
TL;DR: Increased LCFA uptake, reflecting SREBP1c-mediated upregulation of four distinct transporters, is the dominant cause of steatosis in EtOH-fed mice and appears to be essential for full expression of upregulation by insulin.