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首页> 外文期刊>The Journal of Nutritional Biochemistry >Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance
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Reduced delta-6 desaturase activity partially protects against high-fat diet-induced impairment in whole-body glucose tolerance

机译：降低的Delta-6去饱和酶活性部分地保护全身葡萄糖耐受性的高脂饮食诱导的损伤

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摘要

Delta-6 desaturase (D6D), which is encoded by the fatty acid desaturase (Fads2) gene, is the rate-limiting enzyme for the endogenous production of n-3 long-chain polyunsaturated fatty acids. The absence of D6D activity in Fads2(-/-) knockout mice results in the inability to produce eicosapentaenoic acid and docosahexaenoic acid, and has previously been associated with altered glucose and lipid metabolism. Skeletal muscle is a major site for insulin-stimulated glucose disposal; however, the consequences of reduced D6D activity on skeletal muscle metabolism are unknown. The objective of this study was to examine the role of a partial reduction in D6D activity on whole-body glucose tolerance, skeletal muscle fatty acid profiles and protein content of key markers of carbohydrate and fat signaling pathways in the context of both low- and high-fat diets. Male C57BL/6J heterozygous (Fads2(+/-)) and wild-type (WT) mice were fed either a low-fat (16% kcal from fat) or high-fat (HFD; 45% kcal from fat) diet for 21 weeks. Fads2(+/-) mice were protected from the HFD-induced impairment in glucose tolerance. Unexpectedly, HFD-fed Fads2(+/-) mice had reduced GLUT4 skeletal muscle protein content compared to their WT counterparts. No changes were detected in total protein content of key markers of fatty acid uptake, glycogen formation or substrate oxidation. This study shows that reduced D6D activity is partially protective against HFD-induced impairments in whole-body glucose tolerance but does not appear to be due to increased muscle GLUT4 content or total content of proteins regulating substrate utilization. (C) 2019 Elsevier Inc. All rights reserved.
机译：由脂肪酸去饱和酶（FADS2）基因编码的Delta-6去饱和酶（D6D）是用于内源性生产N-3长链多不饱和脂肪酸的速率限制酶。在FADS2（ - / - ）敲除小鼠中没有D6D活性导致不能生产eicosapentaeno的酸和二十二碳六烯酸，并且先前已与改变的葡萄糖和脂质代谢相关。骨骼肌是胰岛素刺激葡萄糖处理的主要部位;然而，D6D活性减少对骨骼肌代谢的后果是未知的。本研究的目的是研究部分减少D6D活性对全身葡萄糖耐量，骨骼肌脂肪酸谱和碳水化合物和脂肪信号传导途径的关键标志物的蛋白质含量的作用，在低和高中 - 饮食。雄性C57BL / 6J杂合（FADS2（+/-））和野生型（WT）小鼠喂养低脂肪（来自脂肪16％Kcal）或高脂肪（HFD; 45％kcal从脂肪）饮食中21周。保护FADS2（+/-）小鼠免受HFD诱导的葡萄糖耐受性的损伤。意外地，与WT对应物相比，HFD喂食的FADS2（+/-）小鼠具有降低的Glut4骨骼肌蛋白质含量。在脂肪酸摄取，糖原形成或基材氧化的关键标志物的总蛋白质含量中没有检测到任何变化。本研究表明，减少的D6D活性在全身葡萄糖耐受性中部分保护抗HFD诱导的损伤，但由于肌肉GLUT4含量增加或蛋白质的总含量调节底物利用的血糖4含量或总含量。 （c）2019 Elsevier Inc.保留所有权利。

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