Abstract

The relationship between conjugated linoleic acid (CLA) and lipogenesis has been extensively studied in mammals and some cell lines, but it is relatively rare in fish, and the potential mechanism of action of CLA reducing fat mass remains unclear. The established primary culture model for studying lipogenesis in grass carp (Ctenopharyngodon idella) preadipocytes was used in the present study, and the objective was to explore the effects of CLA on intracellular lipid and TG content, fatty acid composition, and mRNA levels of adipogenesis transcription factors, lipase, and apoptosis genes in grass carp adipocytes in vitro. The results showed that CLA reduced the size of adipocyte and lipid droplet and decreased the content of intracellular lipid and TG, which was accompanied by a significant down-regulation of mRNA abundance in transcriptional regulators including peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, sterol regulatory element-binding protein (SREBP) 1c, lipase genes including fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), lipoprotein lipase (LPL). Meanwhile, it decreased the content of saturated fatty acids (SFAs) and n − 6 polyunsaturated fatty acid (n-6 PUFA) and increased the content of monounsaturated fatty acid (MUFA) and n − 3 polyunsaturated fatty acid (n-3 PUFA) in primary grass carp adipocyte. In addition, CLA induced adipocyte apoptosis through downregulated anti-apoptotic gene B‐cell CLL/lymphoma 2 (Bcl-2) mRNA level and up-regulated pro-apoptotic genes tumor necrosis factor-α (TNF-α), Bcl-2-associated X protein (Bax), Caspase-3, and Caspase-9 mRNA level in a dose-dependent manner. These findings suggest that CLA can act on grass carp adipocytes through various pathways, including decreasing adipocyte size, altering fatty acid composition, inhibiting adipocyte differentiation, promoting adipocyte apoptosis, and ultimately decreasing lipid accumulation.

中文翻译：

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共轭亚油酸通过下调草鱼（Ctenopharyngodon idella）脂肪细胞脂肪生成基因的表达和上调凋亡基因来减少脂质积累

摘要

共轭亚油酸（CLA）与脂肪生成之间的关系已在哺乳动物和一些细胞系中得到广泛研究，但在鱼类中相对较少，并且 CLA 减少脂肪量的潜在作用机制仍不清楚。本研究采用所建立的草鱼（Ctenopharyngodon idella）前脂肪细胞脂肪生成原代培养模型，探讨CLA对细胞内脂质和TG含量、脂肪酸组成以及脂肪生成转录mRNA水平的影响。草鱼脂肪细胞体外因子、脂肪酶和凋亡基因。结果表明，CLA 减少了脂肪细胞和脂滴的大小，降低了细胞内脂质和 TG 的含量，同时显着下调了过氧化物酶体增殖物激活受体 ( PPAR) γ、CCAAT等转录调节因子的 mRNA 丰度。 /增强子结合蛋白(C/EBP)α、甾醇调节元件结合蛋白(SREBP)1c、脂肪酶基因，包括脂肪酸合酶(FAS)、乙酰辅酶A羧化酶(ACC)、脂蛋白脂肪酶(LPL)。同时，降低了饱和脂肪酸（SFA）和n-6多不饱和脂肪酸（n-6 PUFA）的含量，增加了单不饱和脂肪酸（MUFA）和n-3多不饱和脂肪酸（n-3 PUFA）的含量草鱼原代脂肪细胞中。此外，CLA 通过下调抗凋亡基因 B 细胞 CLL/淋巴瘤 2 ( Bcl-2 ) mRNA 水平和上调促凋亡基因肿瘤坏死因子-α (TNF-α)、Bcl-2- 诱导脂肪细胞凋亡。相关 X 蛋白(Bax)、Caspase-3和Caspase-9 mRNA 水平呈剂量依赖性。这些发现表明，CLA可以通过多种途径作用于草鱼脂肪细胞，包括减少脂肪细胞大小、改变脂肪酸组成、抑制脂肪细胞分化、促进脂肪细胞凋亡，并最终减少脂质积累。