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首页> 外文期刊>American Journal of Physiology >Insulin secretion after dietary supplementation with conjugated linoleic acids and n-3 polyunsaturated fatty acids in normal and insulin-resistant mice.
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Insulin secretion after dietary supplementation with conjugated linoleic acids and n-3 polyunsaturated fatty acids in normal and insulin-resistant mice.

机译：在正常和胰岛素抵抗的小鼠中，日粮中添加共轭亚油酸和n-3多不饱和脂肪酸后，胰岛素分泌会增加。

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摘要

Conjugated linoleic acids (CLAs) and n-3 polyunsaturated fatty acids (PUFAs) improve insulin sensitivity in insulin-resistant rodents. However, the effects of these fatty acids on insulin secretion are not known but are of importance to completely understand their influence on glucose homeostasis. We therefore examined islet function after dietary supplementation consisting of 1% CLAs in combination with 1% n-3 enriched PUFAs for 12 wk to mice on a normal diet and to insulin-resistant mice fed a high-fat diet (58% fat). In the mice fed a normal diet, CLA/PUFA supplementation resulted in insulin resistance associated with low plasma adiponectin levels and low body fat content. Intravenous and oral glucose tolerance tests revealed a marked increase in insulin secretion, which nevertheless was insufficient to counteract the insulin resistance, resulting in glucose intolerance. In freshly isolated islets from mice fed the normal diet, both basal and glucose-stimulated insulin secretion were adaptively augmented by CLA/PUFA, and at a high glucose concentration this was accompanied by elevated glucose oxidation. In contrast, in high-fat-fed mice, CLA/PUFA did not significantly affect insulin secretion, insulin resistance, or glucose tolerance. It is concluded that dietary supplementation of CLA/PUFA in mice fed the normal diet augments insulin secretion, partly because of increased islet glucose oxidation, but that this augmentation is insufficient to counterbalance the induction of insulin resistance, resulting in glucose intolerance. Furthermore, the high-fat diet partly prevents the deleterious effects of CLA/PUFA, but this dietary supplementation was not able to counteract high-fat-diet-induced insulin resistance.
机译：共轭亚油酸（CLA）和n-3多不饱和脂肪酸（PUFA）改善了胰岛素抵抗性啮齿动物的胰岛素敏感性。然而，这些脂肪酸对胰岛素分泌的作用尚不清楚，但对于完全了解其对葡萄糖稳态的影响非常重要。因此，我们在正常饮食的小鼠和高脂饮食（脂肪含量58％）的胰岛素抵抗小鼠中，在12 wk的饮食补充中添加了由1％CLA和1％n-3富集的PUFA组成的膳食补充剂后的胰岛功能。在饲喂正常饮食的小鼠中，补充CLA / PUFA会导致胰岛素抵抗以及血浆脂联素水平低和体脂含量低。静脉和口服葡萄糖耐量试验显示胰岛素分泌显着增加，但仍不足以抵消胰岛素抵抗，导致葡萄糖耐受不良。在用正常饮食喂养的小鼠的新鲜分离的胰岛中，CLA / PUFA可以自适应地增加基础和葡萄糖刺激的胰岛素分泌，在高葡萄糖浓度下，葡萄糖氧化升高。相反，在高脂喂养的小鼠中，CLA / PUFA不会显着影响胰岛素分泌，胰岛素抵抗或葡萄糖耐量。结论是，饲喂正常饮食的小鼠饮食中补充CLA / PUFA可以增加胰岛素分泌，部分原因是由于胰岛葡萄糖氧化增加，但是这种增加不足以抵消胰岛素抵抗的诱导，从而导致葡萄糖耐受不良。此外，高脂饮食部分地防止了CLA / PUFA的有害作用，但这种饮食补充不能抵消高脂饮食诱导的胰岛素抵抗。

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