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 Pelteobagrus fulvidraco. We found that miR-101b directly targeted fatty acid translocase (cd36), caspase9 (casp9) and autophagy-related gene 4A (atg4a). Furthermore, using palmitic acid (PA) or oleic acid (OA) to incubate the primary hepatocytes of yellow catfish, we demonstrated that miR-101b inversely regulated cd36, casp9, and atg4a 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.

中文翻译：

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miR-101b 调节硬骨黄颡鱼 Pelteobagrus fulvidraco 原代肝细胞的脂质沉积和代谢

肝细胞中过多的脂肪沉积，与膳食脂肪摄入过多有关，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，但转录后水平的潜在机制尚不清楚。本研究的目的是探讨miR-101b介导黄鲶Pelteobagrus fulvidraco脂质沉积和代谢的作用和机制。我们发现 miR-101b 直接靶向脂肪酸转位酶 (cd36)、caspase9 (casp9) 和自噬相关基因 4A (atg4a)。此外，使用棕榈酸 (PA) 或油酸 (OA) 培养黄鲶的原代肝细胞，我们证明 miR-101b 在转录水平上反向调节 cd36、casp9 和 atg4a 的表达；miR-101b 的抑制加剧了脂肪酸（FAs、PA 或 OA）诱导的脂质积累，表明 miR-101b 介导了黄鲶中 FAs 诱导的脂质代谢变化。总之，我们的研究为脂质沉积和代谢的调节机制提供了新的见解，并可能为预防和治疗鱼类脂肪肝提供潜在的靶点。