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- W1451032438 abstract "Oxidative stress underlies pathological complication in nonalcoholic fatty liver disease (NAFLD). Heme Oxygenase-1 (HO-1) is a potent endogenous antioxidant gene that plays a key role in decreasing oxidative stress. Sirtuin1 (SIRT1). The aim of this study is to determine whether HO-1 acts through SIRT1 to form a functional module within hepatocytes to attenuate fructose-mediated steatohepatitis and hepatic fibrosis. Effect of fructose, on hepatocyte lipid accumulation and fibrosis in murine hepatocytes and in mice fed a high fructose diet in the presence and absence of CoPP, an inducer of HO-1. Fructose increased heme and decreased HO-1, SIRT1 and pAMPK levels in hepatocytes (p<0.05). Fructose supplementation increased the expression of FAS levels; this increase was negated by CoPP. Concurrent treatment with CoPP and SIRT1 siRNA increased FAS expression suggesting that HO-1 is upstream of SIRT1 and suppression of SIRT1 attenuates the beneficial effects of HO-1. A high fructose diet increased insulin resistance and fibrotic markers in mice (p<0.05). Induction of HO-1 increased SIRT1 levels ameliorated fructose-mediated lipid accumulation and fibrosis in liver (p<0.05 vs. fructose). Taken together, our study demonstrates, that HO-1 induction attenuates fructose-induced hepatic lipid deposition, prevents the development of hepatic fibrosis and abates NAFLD-associated vascular dysfunction. Support NIH Grants HL-55601, HL34300 (N.G.A.)" @default.
- W1451032438 created "2016-06-24" @default.
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- W1451032438 date "2015-04-01" @default.
- W1451032438 modified "2023-10-09" @default.
- W1451032438 title "HO‐1 Induction Attenuates Fructose Mediated Non‐alcoholic Fatty Liver in Hepatocytes and Obese Mice : Involves SIRT1" @default.
- W1451032438 doi "https://doi.org/10.1096/fasebj.29.1_supplement.846.1" @default.
- W1451032438 hasPublicationYear "2015" @default.
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