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10.1038/s41467-018-05309-y http://scihub22266oqcxt.onion/10.1038/s41467-018-05309-y C6048127!6048127!30013137     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=30013137|t=2018. Insulin/Snail1 axis ameliorates fatty liver disease by epigenetically suppressing lipogenesis |pdf=|usr=}}{{30013137}} gab.com Text Insulin/Snail1 axis ameliorates fatty liver disease by epigenetically suppressing lipogenesis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=30013137 #FOAvip Insulin stimulates lipogenesis but insulin resistance is also associated with increased hepatic lipogenesis in obesity. However, the underlying mechanism remains poorly characterized. Here, we show a noncanonical insulin-Snail1 pathway that suppresses lipogenesis. Insulin robustly upregulates zinc-finger protein Snail1 in a PI 3-kinase-dependent manner. In obesity, the hepatic insulin-Snail1 cascade is impaired due to insulin resistance. Hepatocyte-specific deletion of Snail1 enhances insulin-stimulated lipogenesis in hepatocytes, exacerbates dietary NAFLD in mice, and attenuates NAFLD-associated insulin resistance. Liver-specific overexpression of Snail1 has the opposite effect. Mechanistically, Snail1 binds to the fatty acid synthase promoter and recruits HDAC1/2 to induce deacetylation of H3K9 and H3K27, thereby repressing fatty acid synthase promoter activity. Our data suggest that insulin pathways bifurcate into canonical (lipogenic) and noncanonical (anti-lipogenesis by Snail1) two arms. The noncanonical arm counterbalances the canonical arm through Snail1-elicited epigenetic suppression of lipogenic genes. Impairment in the insulin-Snail1 arm may contribute to NAFLD in obesity. Twit Text FOAVip Insulin/Snail1 axis ameliorates fatty liver disease by epigenetically suppressing lipogenesis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=30013137 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30013137 #FOAvip English Wikipedia <ref>{{Cite pmid|30013137}}</ref> Insulin/Snail1 axis ameliorates fatty liver disease by epigenetically suppressing lipogenesis #MMPMID30013137 Liu Y; Jiang L; Sun C; Ireland N; Shah YM; Liu Y; Rui L Nat Commun 2018[]; 9 (ä): ä PMID30013137show ga Insulin stimulates lipogenesis but insulin resistance is also associated with increased hepatic lipogenesis in obesity. However, the underlying mechanism remains poorly characterized. Here, we show a noncanonical insulin-Snail1 pathway that suppresses lipogenesis. Insulin robustly upregulates zinc-finger protein Snail1 in a PI 3-kinase-dependent manner. In obesity, the hepatic insulin-Snail1 cascade is impaired due to insulin resistance. Hepatocyte-specific deletion of Snail1 enhances insulin-stimulated lipogenesis in hepatocytes, exacerbates dietary NAFLD in mice, and attenuates NAFLD-associated insulin resistance. Liver-specific overexpression of Snail1 has the opposite effect. Mechanistically, Snail1 binds to the fatty acid synthase promoter and recruits HDAC1/2 to induce deacetylation of H3K9 and H3K27, thereby repressing fatty acid synthase promoter activity. Our data suggest that insulin pathways bifurcate into canonical (lipogenic) and noncanonical (anti-lipogenesis by Snail1) two arms. The noncanonical arm counterbalances the canonical arm through Snail1-elicited epigenetic suppression of lipogenic genes. Impairment in the insulin-Snail1 arm may contribute to NAFLD in obesity. äInsulin/Snail1 axis ameliorates fatty liver disease by epigenetically (epmc).pdf DeepDyve Pubget Overpricing