Global deficiency of stearoyl-CoA desaturase-2 protects against diet-induced adiposity.
Global deficiency of stearoyl-CoA desaturase-2 protects against diet-induced adiposity.
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硬脂酰辅酶 A 去饱和酶 2 的整体缺乏可预防饮食引起的肥胖。
DOI：
10.1016/j.bbrc.2020.04.077
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发表时间：
2020
影响因子：
3.1
通讯作者：
Ntambi,JamesM
中科院分区：
文献类型：
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作者：
O'Neill,LucasM;Phang,YarXin;Matango,Majaliwa;Shamsuzzaman,Sohel;Guo,Chang-An;Nelson,DavidW;Yen,Chi-LiangE;Ntambi,JamesM
在小鼠中，有四种硬脂酰辅酶A去饱和酶亚型（SCD1-4）可催化单不饱和脂肪酸的合成。此前，我们已经证明，全身 SCD1 亚型缺失 (SCD1KO) 的小鼠可以免受饮食和遗传性肥胖的影响。在这里，我们报告说，SCD2亚型（SCD2KO）的整体删除对高脂肪饮食（HFD）和高碳水化合物饮食（HCD）引起的肥胖的发生提供了类似的保护作用。 HFD 喂养 10 周或 HCD 喂养 6 周后，SCD2KO 小鼠体重未能增加，脂肪量减少。在 HFD 治疗中，SCD2KO 小鼠仍保持葡萄糖和胰岛素耐受性。最后，高脂饮食喂养的 SCD2KO 小鼠的棕色脂肪组织中能量消耗标志物 UCP1 和 PGC-1α 增加。
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.