Wang Yanli, Li Xin, Cao Yang, Xiao Cheng, Liu Yu, Jin Haiguo, Cao Yang
Institute of Animal Biotechnology, Jilin Academy of Agricultural Science, Changchun, China.
Institute of Animal Husbandry and Veterinary, Zhejiang Academy of Agricultural Sciences, Hangzhou, China.
Front Genet. 2021 Jun 21;12:649140. doi: 10.3389/fgene.2021.649140. eCollection 2021.
Acetyl-CoA acyltransferase 1 () functions as a key regulator of fatty acid β-oxidation in peroxisomes by catalyzing the cleavage of 3-ketoacyl-CoA to acetyl-CoA and acyl-CoA, which participate in the extension and degradation of fatty acids. Thus, is an important regulator of lipid metabolism and plays an essential role in fatty acid oxidation and lipid metabolism. Our previous study findings revealed that is closely associated with the peroxisome proliferator-activated receptor () signaling and fatty acid metabolism pathways, which are involved in fat deposition in sheep, leading to our hypothesis that may be involved in fat deposition by regulating lipid metabolism. However, the associated molecular mechanism remains unclear. In the present study, to assess the potential function of in sheep preadipocyte differentiation, we knocked down and overexpressed in sheep preadipocytes and evaluated the pattern of gene expression during preadipocyte differentiation by qRT-PCR. was significantly expressed in the early stage of adipocyte differentiation, and then its expression decreased. deficiency increased lipid accumulation and the triglyceride content and promoted sheep preadipocyte differentiation, whereas overexpression inhibited adipogenesis and decreased lipid accumulation and the triglyceride content. Simultaneously, we demonstrated that deficiency upregulated the expressions of the adipogenic marker genes γ and α in sheep preadipocytes, but overexpression inhibited the expressions of these markers, indicating that affects lipid metabolism by regulating adipogenic marker genes. Our results may promote a better understanding of the regulation of adipogenesis by .
乙酰辅酶A酰基转移酶1()通过催化3-酮酰基辅酶A裂解为乙酰辅酶A和酰基辅酶A,在过氧化物酶体中作为脂肪酸β-氧化的关键调节因子,这两种物质参与脂肪酸的延长和降解。因此,是脂质代谢的重要调节因子,在脂肪酸氧化和脂质代谢中起重要作用。我们之前的研究结果表明,与过氧化物酶体增殖物激活受体()信号通路和脂肪酸代谢途径密切相关,这些途径参与绵羊的脂肪沉积,由此我们推测可能通过调节脂质代谢参与脂肪沉积。然而,相关的分子机制仍不清楚。在本研究中,为了评估在绵羊前体脂肪细胞分化中的潜在功能,我们在绵羊前体脂肪细胞中敲低和过表达,并通过qRT-PCR评估前体脂肪细胞分化过程中的基因表达模式。在脂肪细胞分化的早期显著表达,然后其表达下降。缺乏增加了脂质积累和甘油三酯含量,并促进了绵羊前体脂肪细胞的分化,而过表达则抑制脂肪生成并降低脂质积累和甘油三酯含量。同时,我们证明缺乏上调了绵羊前体脂肪细胞中脂肪生成标记基因γ和α的表达,但过表达抑制了这些标记物的表达,表明通过调节脂肪生成标记基因影响脂质代谢。我们的结果可能有助于更好地理解对脂肪生成的调节作用。