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首页> 外文期刊>American Journal of Physiology >Loss of stearoyl-CoA desaturase 1 inhibits fatty acid oxidation and increases glucose utilization in the heart
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Loss of stearoyl-CoA desaturase 1 inhibits fatty acid oxidation and increases glucose utilization in the heart

机译：硬脂酰辅酶A去饱和酶1的丢失会抑制脂肪酸氧化并增加心脏中的葡萄糖利用率

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First published November 27, 2007; doj:10.1152/ajpendo.00471.2007.-Stearoyl-CoA desaturase (SCD) is a lipogenic enzyme that catalyzes the synthesis of monounsaturated fatty acids (FA). SCD1 deficiency activates metabolic pathways that promote FA beta-oxidation and decrease lipogenesis in liver. In the present study, we show that FA transport and oxidation are decreased, whereas glucose uptake and oxidation are increased in the heart of SCDl~(-/-) mice. Protein levels of FA transport proteins such as FA translocase/CD36 and FA transport protein as well as activity of carnitine palmitoyltransferase 1, the rate-limiting enzyme for mitochondrial fat oxidation, were significantly lower in the heart of SCDl~(-/-) mice compared with SCD1~(+/+) mice. Consequently, the rate of palmitoyl-CoA oxidation was decreased significantly in the heart of SCD I~(-/-) mice. mRNA levels of peroxisome proliferator-activated receptor-a, a key transcription factor controlling genes of FA oxidation, were significantly reduced inSCD 1~(-/-) mice. Phosphorylation of insulin receptor substrate~(-1) (TRS~(-1)) and the association of ap85 subunit of phosphatidylinositol 3-kinase with IRS~(-1) were significantly higher under both basal and insulin-stimulated conditions in SCDl~(-/-) hearts. This increased insulin sensitivity translated to a 1.8-fold greater 2-deoxyglucose uptake and 2-fold higher rate of glucose oxidation in the myocardium compared with SCD1~(+/+) counterparts. The results suggest that SCD1 deficiency causes a shift in cardiac substrate utilization from FA to glucose by upregulating insulin signaling, decreasing FA availability, and reducing expression of FA oxidation genes in the heart. This increase in cardiac insulin sensitivity and glucose utilization due to SCD1 deficiency could prove therapeutic in pathological conditions such as obesity that are characterized by skewed cardiac substrate utilization.
机译：首次发布于2007年11月27日; doj：10.1152 / ajpendo.00471.2007.-硬脂酰辅酶A去饱和酶（SCD）是一种脂肪生成酶，可催化单不饱和脂肪酸（FA）的合成。 SCD1缺乏会激活代谢途径，从而促进FAβ氧化并减少肝脏中的脂肪生成。在本研究中，我们显示SCD1〜（-/-）小鼠心脏中的FA转运和氧化减少，而葡萄糖摄取和氧化增加。在SCD1〜（-/-）小鼠的心脏中，FA转运蛋白（例如FA转运酶/ CD36和FA转运蛋白）的蛋白水平以及肉碱棕榈酰转移酶1（线粒体脂肪氧化的限速酶）的活性显着降低。与SCD1〜（+ / +）小鼠相比。因此，SCD I〜（-/-）小鼠心脏中棕榈酰-CoA氧化速率显着降低。在SCD 1〜（-/-）小鼠中，过氧化物酶体增殖物激活受体-α（FA氧化的关键转录因子控制基因）的mRNA水平显着降低。在基础和胰岛素刺激的条件下，在SCD1〜中，胰岛素受体底物〜（-1）（TRS〜（-1））的磷酸化以及磷脂酰肌醇3-激酶的ap85亚基与IRS〜（-1）的关联均显着更高。 （-/-）心。与SCD1〜（+ / +）对应物相比，这种增加的胰岛素敏感性转化为心肌中2-脱氧葡萄糖摄取增加了1.8倍，葡萄糖氧化速率增加了2倍。结果表明，SCD1缺乏会通过上调胰岛素信号传导，减少FA的可利用性以及减少心脏中FA氧化基因的表达而导致心脏底物利用从FA转移至葡萄糖。由于SCD1缺乏引起的心脏胰岛素敏感性和葡萄糖利用的增加，可以证明在以肥胖的基质为特征的病理性疾病（例如肥胖）中具有治疗作用。

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