Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI, 53706, USA.
Department of Nutritional Sciences, University of Wisconsin-Madison, 1415 Linden Drive, Madison, WI, 53706, USA.
Biochem Biophys Res Commun. 2020 Jun 30;527(3):589-595. doi: 10.1016/j.bbrc.2020.04.077. Epub 2020 May 15.
In mouse, there are four stearoyl-CoA desaturase isoforms (SCD1-4) that catalyze the synthesis of monounsaturated fatty acids. Previously, we have shown that mice harboring a whole body deletion of the SCD1 isoform (SCD1KO) are protected from diet and genetically induced adiposity. Here, we report that global deletion of the SCD2 isoform (SCD2KO) provides a similar protective effect against the onset of both high-fat diet (HFD) and high-carbohydrate diet (HCD) induced adiposity. After 10 weeks of HFD feeding or 6 weeks of HCD feeding, SCD2KO mice failed to gain weight and had decreased fat mass. On HFD, SCD2KO mice remained glucose and insulin tolerant. Lastly, the markers for energy expenditure, UCP1 and PGC-1α, were increased in the brown adipose tissue of HFD fed SCD2KO mice.
在小鼠中,有四种硬脂酰辅酶 A 去饱和酶同工型(SCD1-4),它们催化单不饱和脂肪酸的合成。以前,我们已经表明,全身缺失 SCD1 同工型(SCD1KO)的小鼠可以预防饮食和遗传诱导的肥胖。在这里,我们报告称,SCD2 同工型(SCD2KO)的全局缺失对高脂肪饮食(HFD)和高碳水化合物饮食(HCD)诱导的肥胖的发生提供了类似的保护作用。在 HFD 喂养 10 周或 HCD 喂养 6 周后,SCD2KO 小鼠体重没有增加,脂肪量减少。在 HFD 上,SCD2KO 小鼠仍然对葡萄糖和胰岛素耐受。最后,在 HFD 喂养的 SCD2KO 小鼠的棕色脂肪组织中,能量消耗标志物 UCP1 和 PGC-1α 增加。