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• W4220886055 abstract "Abstract There is increasing evidence for the importance of the nuclear envelope in lipid metabolism, nonalcoholic fatty liver disease (NAFLD), and nonalcoholic steatohepatitis (NASH). Human mutations in LMNA , encoding A-type nuclear lamins, cause early-onset insulin resistance and NASH, while hepatocyte-specific deletion of Lmna predisposes to NASH with fibrosis in male mice. Given that variants in the gene encoding LAP2α, a nuclear protein that regulates lamin A/C, were previously identified in patients with NAFLD, we sought to determine the role of LAP2α in NAFLD using a mouse genetic model. Hepatocyte-specific Lap2a-knockout ( Lap2α (ΔHep) ) mice and littermate controls were fed normal chow or high-fat diet (HFD) for 8 weeks or 6 months. In contrast to what was observed with hepatocyte-specific Lmna deletion, male Lap2a (ΔHep) mice showed no increase in hepatic steatosis or NASH compared to controls. Rather, Lap2a (ΔHep) mice demonstrated reduced hepatic steatosis, particularly after long-term HFD, with decreased susceptibility to diet-induced NASH. Accordingly, whereas pro-steatotic genes Cidea, Mogat1 , and Cd36 were upregulated in Lmnα -KO mice, they were downregulated in Lap2α (ΔHep) mice, and there was a trend toward decreases in pro-inflammatory and pro-fibrotic genes. These data indicate that hepatocyte-specific Lap2a deletion protects against hepatic steatosis and NASH in mice; therefore, LAP2α might represent a potential therapeutic target in human NASH. Brief Summary Loss of LAP2α in mouse hepatocytes protected against diet-induced hepatic steatosis and NASH." @default.
• W4220886055 created "2022-04-03" @default.
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• W4220886055 date "2022-03-19" @default.
• W4220886055 modified "2023-10-17" @default.
• W4220886055 title "Hepatocyte-specific loss of LAP2α protects against diet-induced hepatic steatosis and steatohepatitis in male mice" @default.
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• W4220886055 doi "https://doi.org/10.1101/2022.03.18.484917" @default.
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