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miR-101b Regulates Lipid Deposition and Metabolism of Primary Hepatocytes in Teleost Yellow Catfish Pelteobagrus fulvidraco

机译:miR-101b调节眼肝细胞中肝细胞的脂质沉积和代谢在Textost黄色的鲶鱼pelteobagrus fulvidraco中

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摘要

Excessive fat deposition in the hepatocytes, associated with excess dietary fat intake, was related to the occurrence of fatty livers in fish. miR-101b plays the important roles in controlling lipid metabolism, but the underlying mechanism at the post-transcriptional level remains unclear. The purpose of this study is to explore the roles and mechanism of miR-101b-mediating lipid deposition and metabolism in yellow catfish . We found that miR-101b directly targeted fatty acid translocase ( ), caspase9 ( ) and autophagy-related gene 4A ( ). Furthermore, using palmitic acid (PA) or oleic acid (OA) to incubate the primary hepatocytes of yellow catfish, we demonstrated that miR-101b inversely regulated , and expression at the transcriptional level; the inhibition of miR-101b aggravated fatty acids (FAs, PA or OA)-induced lipid accumulation, indicating that miR-101b mediated FAs-induced variations of lipid metabolism in yellow catfish. Taken together, our study gave novel insight into the regulatory mechanism of lipid deposition and metabolism and might provide potential targets for the prevention and treatment of fatty livers in fish.
机译:与过量膳食脂肪摄入相关的肝细胞中过度脂肪沉积与鱼类脂肪肝的发生有关。 miR-101b在控制脂质代谢中起重要作用,但后转录水平的潜在机制仍然不清楚。本研究的目的是探讨miR-101b介导的脂质沉积和黄色鲶鱼代谢的作用和机制。我们发现miR-101b直接靶向脂肪酸易转化酶(),caspase9()和自噬相关基因4a()。此外,使用棕榈酸(PA)或油酸(OA)孵育黄鲶的原发性肝细胞,我们证明MIR-101B逆转地调节,并在转录水平上表达;抑制miR-101b加重脂肪酸(Fas,pa或Oa)诱导的脂质积累,表明miR-101b介导的Fas致血液代谢变异在黄色鲶鱼中。我们的研究占据了新颖的洞察脂沉积和新陈代谢的调节机制,并且可以为鱼类中的防治和治疗脂肪肝的潜在目标提供潜在的目标。

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