Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity
Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity
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DOI：
10.1073/pnas.132384699
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发表时间：
2002-08-20
影响因子：
11.1
通讯作者：
Attie, AD
中科院分区：
文献类型：
--
作者：
Ntambi, JM;Miyazaki, M;Attie, AD
硬脂酰辅酶A去饱和酶（SCD）是催化单不饱和脂肪酸（主要是油酸酯（C18：1）和棕榈油酸酯（C16：11））合成的中心脂肪生成酶，所述单不饱和脂肪酸是膜磷脂、甘油三酯、蜡酯和胆固醇酯的组分。在小鼠中存在几种SCID同种型（SCD 1 -3）。在这里，我们表明，有针对性地破坏SCD 1亚型的小鼠减少了身体肥胖，增加了胰岛素敏感性，并抵抗饮食诱导的体重增加。防止肥胖涉及增加能量消耗和增加氧气消耗。与野生型小鼠相比，SCD 1-/-小鼠的血浆酮体水平升高，但血浆胰岛素和瘦素水平降低。在SCD 1-/-小鼠中，几个脂质氧化基因的表达上调，而脂质合成基因下调。这些观察结果表明，SCD 1缺乏的后果是除了减少甘油三酯合成和储存外，还激活了脂质氧化。
Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:11), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCID isoforms (SCD1-3) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1-/- mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1-/- mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage.