Metabolic Disease Research Center, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
Department of Obstetrics and Gynecology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
Adipocyte. 2023 Dec;12(1):2173966. doi: 10.1080/21623945.2023.2173966.
Low meat performance is the defect of Small Tail Han sheep. Intramuscular fat affects meat quality and largely determined by adipogenesis. In previous study, miR136 was showed one of differentially expressed microRNAs between preadipocytes and mature adipocytes of Small Tail Han sheep but its role in adipogenesis is still not elucidated. Here, we investigated the effect of miR136 on adipogenesis and the underlying mechanism. qPCR data showed that miR136 level increased with preadipocytes proliferation while declined with preadipocytes differentiation. Moreover, miR136 mimics blocked lipid droplet formation, reduced lipid content and triglyceride accumulation while miR136 inhibitor showed the opposite effects, revealing that miR136 promoted preadipocytes proliferation but inhibited preadipocytes differentiation. Bioinformatics and biochemical validation manifested that PPARGC1B was a target of miR136. Furthermore, miR136 mimics decreased PPARγ and C/EBPα expression accompanied by PPARGC1B expression descending. Reverse effects were observed with miR136 inhibitor. Besides, overexpression of miR136 elevated IGF1 expression. Collectively, our data first exhibited a regulatory role of miR136 in adipogenesis, which is promoting preadipocytes proliferation through elevating IGF1 expression while inhibiting preadipocytes differentiation through targeting PPARGC1B and further declined PPARγ and C/EBPα expression. The modulation of PPARGC1B by miR136 may provide a new potential target for increasing intramuscular fat.
低产肉性能是小尾寒羊的缺陷。肌内脂肪影响肉质，主要由脂肪生成决定。在之前的研究中，miR136 被证明是小尾寒羊前体脂肪细胞和成熟脂肪细胞之间差异表达的 microRNA 之一，但它在脂肪生成中的作用仍未阐明。在这里，我们研究了 miR136 对脂肪生成的影响及其潜在机制。qPCR 数据显示，miR136 水平随着前体脂肪细胞的增殖而增加，随着前体脂肪细胞的分化而下降。此外，miR136 模拟物阻断了脂滴的形成，减少了脂质含量和甘油三酯的积累，而 miR136 抑制剂则表现出相反的效果，表明 miR136 促进了前体脂肪细胞的增殖，但抑制了前体脂肪细胞的分化。生物信息学和生化验证表明，PPARGC1B 是 miR136 的靶标。此外，miR136 模拟物降低了 PPARγ 和 C/EBPα 的表达，同时伴随着 PPARGC1B 的表达下降。miR136 抑制剂则观察到相反的效果。此外，miR136 过表达提高了 IGF1 的表达。综上所述，我们的数据首次展示了 miR136 在脂肪生成中的调节作用，它通过提高 IGF1 的表达来促进前体脂肪细胞的增殖，通过靶向 PPARGC1B 并进一步降低 PPARγ 和 C/EBPα 的表达来抑制前体脂肪细胞的分化。miR136 对 PPARGC1B 的调节可能为增加肌内脂肪提供了一个新的潜在靶点。
