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10.1172/JCI89934 http://scihub22266oqcxt.onion/10.1172/JCI89934 C5490767!5490767 !28628040     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28628040 &cmd=llinks): Failed to open stream: HTTP request failed! 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Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity |pdf=|usr=}}{{28628040 }} gab.com Text Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28628040 #FOAvip Epidemiologic and animal studies implicate overconsumption of fructose in the development of nonalcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remain largely unknown. Here, we have presented evidence supporting the essential function of the lipogenic transcription factor carbohydrate response element-binding protein (ChREBP) in mediating adaptive responses to fructose and protecting against fructose-induced hepatotoxicity. In WT mice, a high-fructose diet (HFrD) activated hepatic lipogenesis in a ChREBP-dependent manner; however, in Chrebp-KO mice, a HFrD induced steatohepatitis. In Chrebp-KO mouse livers, a HFrD reduced levels of molecular chaperones and activated the C/EBP homologous protein-dependent (CHOP-dependent) unfolded protein response, whereas administration of a chemical chaperone or Chop shRNA rescued liver injury. Elevated expression levels of cholesterol biosynthesis genes in HFrD-fed Chrebp-KO livers were paralleled by an increased nuclear abundance of sterol regulatory element-binding protein 2 (SREBP2). Atorvastatin-mediated inhibition of hepatic cholesterol biosynthesis or depletion of hepatic Srebp2 reversed fructose-induced liver injury in Chrebp-KO mice. Mechanistically, we determined that ChREBP binds to nuclear SREBP2 to promote its ubiquitination and destabilization in cultured cells. Therefore, our findings demonstrate that ChREBP provides hepatoprotection against a HFrD by preventing overactivation of cholesterol biosynthesis and the subsequent CHOP-mediated, proapoptotic unfolded protein response. Our findings also identified a role for ChREBP in regulating SREBP2-dependent cholesterol metabolism. Twit Text FOAVip Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28628040 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28628040 #FOAvip English Wikipedia <ref>{{Cite pmid|28628040 }}</ref> Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity #MMPMID28628040 Zhang D ; Tong X ; VanDommelen K ; Gupta N ; Stamper K ; Brady GF ; Meng Z ; Lin J ; Rui L ; Omary MB ; Yin L J Clin Invest 2017[Jun]; 127 (7 ): 2855-2867 PMID28628040 show ga Epidemiologic and animal studies implicate overconsumption of fructose in the development of nonalcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remain largely unknown. Here, we have presented evidence supporting the essential function of the lipogenic transcription factor carbohydrate response element-binding protein (ChREBP) in mediating adaptive responses to fructose and protecting against fructose-induced hepatotoxicity. In WT mice, a high-fructose diet (HFrD) activated hepatic lipogenesis in a ChREBP-dependent manner; however, in Chrebp-KO mice, a HFrD induced steatohepatitis. In Chrebp-KO mouse livers, a HFrD reduced levels of molecular chaperones and activated the C/EBP homologous protein-dependent (CHOP-dependent) unfolded protein response, whereas administration of a chemical chaperone or Chop shRNA rescued liver injury. Elevated expression levels of cholesterol biosynthesis genes in HFrD-fed Chrebp-KO livers were paralleled by an increased nuclear abundance of sterol regulatory element-binding protein 2 (SREBP2). Atorvastatin-mediated inhibition of hepatic cholesterol biosynthesis or depletion of hepatic Srebp2 reversed fructose-induced liver injury in Chrebp-KO mice. Mechanistically, we determined that ChREBP binds to nuclear SREBP2 to promote its ubiquitination and destabilization in cultured cells. Therefore, our findings demonstrate that ChREBP provides hepatoprotection against a HFrD by preventing overactivation of cholesterol biosynthesis and the subsequent CHOP-mediated, proapoptotic unfolded protein response. Our findings also identified a role for ChREBP in regulating SREBP2-dependent cholesterol metabolism. |Animals [MESH] |Basic Helix-Loop-Helix Leucine Zipper Transcription Factors [MESH] |Chemical and Drug Induced Liver Injury/genetics/*metabolism/pathology [MESH] |Cholesterol/genetics/metabolism [MESH] |Dietary Carbohydrates/*adverse effects/pharmacology [MESH] |Fructose/*adverse effects/pharmacology [MESH] |Liver/injuries/*metabolism/pathology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |Protein Binding/drug effects/genetics [MESH] |Sterol Regulatory Element Binding Protein 2/genetics/metabolism [MESH] |Transcription Factors/genetics/*metabolism [MESH]Lipogenic transcription factor ChREBP mediates fructose-induced metabo(epmc).pdf DeepDyve Pubget Overpricing