Why the study?
Does knockdown of MALAT1 prevent hepatic lipid accumulation and insulin resistance in ob/ob mice and HepG2 cells?
Does knockdown of MALAT1 prevent hepatic lipid accumulation and insulin resistance in ob/ob mice and HepG2 cells?
MALAT1 promotes hepatic steatosis and insulin resistance by increasing nuclear SREBP-1c protein stability, highlighting a potential therapeutic target for metabolic disorders.
MALAT1 knockdown shows promise in obese mouse models; leaves open whether targeting MALAT1 benefits patients with hepatic steatosis.
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is implicated in liver cell proliferation. However, its role in hepatic steatosis and insulin resistance remain poorly understood. The aim of this study was to investigate the effects of MALAT1 on hepatic lipid accumulation and its potential targets. As expected, MALAT1 expression is increased in hepatocytes exposed to palmitate and livers of ob/ob mice. Knockdown of MALAT1 expression dramatically suppressed palmitate-induced lipid accumulation and the increase of nuclear SREBP-1c protein in HepG2 cells. In addition, RNA immunoprecipitation and RNA pull-down assay confirmed that MALAT1 interacted with SREBP-1c to stabilize nuclear SREBP-1c protein. Finally, injection of si-MALAT1 prevented hepatic lipid accumulation and insulin resistance in ob/ob mice. In conclusion, our observations suggest that MALAT1 promotes hepatic steatosis and insulin resistance by increasing nuclear SREBP-1c protein stability.
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Yan et al. (2016) studied this question.
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