Kadegowda A K G, Burns T A, Pratt S L, Duckett S K
Clemson University, Clemson, SC, USA.
Lipids. 2013 Oct;48(10):967-76. doi: 10.1007/s11745-013-3823-1. Epub 2013 Aug 9.
The objectives were to determine the effect of stearoyl-CoA desaturase (SCD1) inhibition on adipocyte proliferation, differentiation and cellular lipid metabolism in bovine primary adipocytes. Inhibition of SCD1 activity by sterculic acid (SA) or conjugated linoleic acid, trans-10 cis-12 isomer, (t10, c12-CLA) did not alter adipocyte cellular proliferation, viability or differentiation. In 1,2-[(13)C]-acetate supplemented cells, the mass isotopomer distribution analysis showed that the fractional synthesis rate of [(13)C]-16:0 was reduced (P < 0.01) in SA and t10, c12-CLA treatments compared to control. Of the lipogenic genes, t10, c12-CLA treatment decreased (P < 0.05) the expression of SCD1, acetyl-CoA carboxylase (ACC), fatty acid synthase; whereas SA supplementation decreased (P < 0.05) the expression of ACC. Both SA and t10, c12-CLA increased (P < 0.05) the expression of hormone-sensitive lipase and carnitine palmitoyl transferase involved in lipolysis and oxidation. Inhibition of SCD1 in bovine adipocytes decreases de novo fatty acid synthesis by down-regulating genes involved in lipogenesis and up-regulating genes involved in lipolysis and oxidation.
本研究旨在确定硬脂酰辅酶A去饱和酶（SCD1）抑制对牛原代脂肪细胞中脂肪细胞增殖、分化及细胞脂质代谢的影响。用苹婆酸（SA）或共轭亚油酸反式-10顺式-12异构体（t10，c12-CLA）抑制SCD1活性，并未改变脂肪细胞的增殖、活力或分化。在添加1,2-[(13)C]-乙酸盐的细胞中，质量同位素异构体分布分析表明，与对照相比，SA和t10，c12-CLA处理组中[(13)C]-16:0的分数合成率降低（P<0.01）。在生脂基因中，t10，c12-CLA处理降低了（P<0.05）SCD1、乙酰辅酶A羧化酶（ACC）、脂肪酸合酶的表达；而添加SA降低了（P<0.05）ACC的表达。SA和t10，c12-CLA均增加了（P<0.05）参与脂解和氧化过程的激素敏感性脂肪酶和肉碱棕榈酰转移酶的表达。抑制牛脂肪细胞中的SCD1可通过下调参与脂肪生成的基因和上调参与脂解和氧化的基因来减少脂肪酸的从头合成。
