Yu Hua, Zou Zhao-Xia, Wei Wei, Li Ying
College of Life Science, Chongqing Normal University, Chongqing, 400047, People's Republic of China.
Mar Biotechnol (NY). 2024 Feb;26(1):169-180. doi: 10.1007/s10126-024-10286-z. Epub 2024 Jan 15.
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.
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，CLA降低脂肪量的潜在作用机制仍不清楚。本研究采用已建立的草鱼（Ctenopharyngodon idella）前脂肪细胞脂肪生成研究原代培养模型，目的是探讨CLA对草鱼脂肪细胞内脂质和甘油三酯（TG）含量、脂肪酸组成以及脂肪生成转录因子、脂肪酶和凋亡基因mRNA水平的影响。结果表明，CLA减小了脂肪细胞和脂滴的大小，降低了细胞内脂质和TG的含量，同时伴随着转录调节因子过氧化物酶体增殖物激活受体（PPAR）γ、CCAAT/增强子结合蛋白（C/EBP）α、固醇调节元件结合蛋白（SREBP）1c以及脂肪酶基因脂肪酸合酶（FAS）、乙酰辅酶A羧化酶（ACC）、脂蛋白脂肪酶（LPL）mRNA丰度的显著下调。同时，它降低了原代草鱼脂肪细胞中饱和脂肪酸（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。此外，CLA通过下调抗凋亡基因B细胞淋巴瘤/白血病-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相关X蛋白（Bax）、半胱天冬酶-3（Caspase-3）和半胱天冬酶-9（Caspase-9）mRNA水平，以剂量依赖的方式诱导脂肪细胞凋亡。这些发现表明，CLA可通过多种途径作用于草鱼脂肪细胞，包括减小脂肪细胞大小、改变脂肪酸组成、抑制脂肪细胞分化、促进脂肪细胞凋亡，最终减少脂质积累。
