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Dietary nitrite supplementation improves insulin resistance in type 2 diabetic KKAy mice

机译:膳食亚硝酸盐补充剂改善了2型糖尿病KKay小鼠的胰岛素抵抗力

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摘要

Background Because insulin signaling is essential for endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) production, the loss of bioavailable NO might be a common molecular mechanism underlying the development of insulin resistance and endothelial dysfunction. Although dietary nitrite acts as a substrate for systemic NO generation, thereby serving as a physiological alternative source of NO for signaling, it is not precisely known how dietary nitrite affects type 2 diabetes mellitus. Here we report the therapeutic effects of dietary nitrite on the metabolic and histological features of KKAy diabetic mice. Methods KKAy mice were divided into three groups (without nitrite, and with 50 mg/L and 150 mg/L nitrite in drinking water), and two groups of C57BL/6J mice served as controls (without nitrite and with 150 mg/L nitrite in drinking water). After 10 weeks, blood samples, visceral adipose tissues, and gastrocnemius muscles were collected after a 16-hour fast to assess the homeostasis model assessment of insulin resistance (HOMA-IR) levels, the histology of the adipose tissue, insulin-stimulated sequential signaling to glucose transporter 4 (GLUT4), and nitrite and nitrate contents in the muscle using an HPLC system. Results KKAy mice developed obesity with enhanced fasting plasma levels of glucose and insulin and exhibited increased HOMA-IR scores compared with the C57BL/6J control mice. Dietary nitrite dose-dependently reduced the size of the hypertrophic adipocytes and TNF-α transcription in the adipose tissue of KKAy diabetic mice, which also restored the insulin-mediated signal transduction, including p85 and Akt phosphorylation, and subsequently restored the GLUT4 expression in the skeletal muscles. Conclusions These results suggest that dietary nitrite provides an alternative source of NO, and subsequently improves the insulin-mediated signaling and the metabolic and histological features in KKAy diabetic mice.
机译:背景技术由于胰岛素信号传导对于内皮一氧化氮合酶(ENOS)强化一氧化氮(NO)产生,因此生物可利用率的损失可能是胰岛素抵抗和内皮功能障碍发育的常见分子机制。虽然膳食亚硝酸盐作为全身产生的基材,但是用作用于信号传导的NO的生理替代来源,尤其是亚硝酸盐如何影响2型糖尿病。在这里,我们报告了膳食亚硝酸盐对KKay糖尿病小鼠代谢和组织学特征的治疗作用。方法将KKay小鼠分为三组(无亚硝酸盐,饮用水中50mg / L和150mg / L亚硝酸盐),以及两组C57BL / 6J小鼠用作对照(无亚硝酸盐和150mg / L亚硝酸盐在饮用水中)。经过10周后,在快速16小时后收集血液样本,内脏脂肪组织和腓肠肌肌肉,以评估胰岛素抵抗(HOMA-IR)水平的稳态模型评估,脂肪组织的组织学,胰岛素刺激的连续信令使用HPLC系统在肌肉中葡萄糖转运蛋白4(Glut4)和亚硝酸盐和硝酸盐含量。结果KKAY小鼠通过增强的葡萄糖和胰岛素的葡萄糖和胰岛素产生肥胖,并与C57BL / 6J对照小鼠相比,HOMA-IR分数增加。膳食亚硝酸盐剂量依赖性降低了KKay糖尿病小鼠的脂肪组织中的肥厚性脂肪细胞和TNF-α转录的大小,这也恢复了胰岛素介导的信号转导,包括P85和AKT磷酸化,随后恢复了GLUT4表达骨骼肌。结论这些结果表明,膳食亚硝酸盐提供了替代源,随后改善了胰岛素介导的信号传导和KKay糖尿病小鼠中的代谢和组织学特征。

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