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谷氨酸单钠肥胖小鼠的游泳训练可改善胰岛中胰岛素受体酪氨酸磷酸化的损伤。

Swim training of monosodium L-glutamate-obese mice improves the impaired insulin receptor tyrosine phosphorylation in pancreatic islets.

机构信息

Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá/UEM, Block H67, Room 19, Avenue Colombo, 5790, Maringá, PR, 87020-900, Brazil.

出版信息

Endocrine. 2013 Jun;43(3):571-8. doi: 10.1007/s12020-012-9798-5. Epub 2012 Sep 16.

DOI:10.1007/s12020-012-9798-5
PMID:22983867
Abstract

The goal of the present study was to investigate changes on glucose homoeostasis and of the insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) signalling in pancreatic islets from MSG-obese mice submitted to or not submitted to swim training. Swim training of 90-day-old MSG mice was used to evaluate whether signalling pathways of the IR and IRS-1 in islets are involved with the insulin resistance and glucose intolerance observed in this obese animal model. The results showed that IR tyrosine phosphorylation (pIR) was reduced by 42 % in MSG-obese mice (MSG, 6.7 ± 0.2 arbitrary units (a.u.); control, 11.5 ± 0.4 a.u.); on the other hand, exercise training increased pIR by 76 % in MSG mice without affecting control mice (MSG, 11.8 ± 0.3; control, 12.8 ± 0.2 a.u.). Although the treatment with MSG increased IRS-1 tyrosine phosphorylation (pIRS-1) by 96 % (MSG, 17.02 ± 0.6; control, 8.7 ± 0.2 a.u.), exercise training also increased it in both groups (control, 13.6 ± 0.1; MSG, 22.2 ± 1.1 a.u.). Current research shows that the practice of swim training increases the tyrosine phosphorylation of IRS-1 which can modulate the effect caused by obesity in insulin receptors.

摘要

本研究的目的是探讨肥胖症模型小鼠胰岛中葡萄糖稳态和胰岛素受体(IR)及胰岛素受体底物-1(IRS-1)信号转导的变化,以及游泳训练是否对此有影响。通过对 90 日龄肥胖症模型小鼠进行游泳训练,评估胰岛中 IR 和 IRS-1 的信号通路是否与该肥胖动物模型中观察到的胰岛素抵抗和葡萄糖耐量受损有关。结果表明,肥胖症模型小鼠的 IR 酪氨酸磷酸化(pIR)降低了 42%(MSG,6.7±0.2 任意单位(a.u.);对照组,11.5±0.4 a.u.);另一方面,运动训练使 MSG 组的 pIR 增加了 76%,而对对照组没有影响(MSG,11.8±0.3;对照组,12.8±0.2 a.u.)。尽管肥胖症模型小鼠的 IRS-1 酪氨酸磷酸化(pIRS-1)增加了 96%(MSG,17.02±0.6;对照组,8.7±0.2 a.u.),但运动训练也使两组的 pIRS-1 都增加了(对照组,13.6±0.1;MSG,22.2±1.1 a.u.)。目前的研究表明,游泳训练可以增加 IRS-1 的酪氨酸磷酸化,从而调节肥胖对胰岛素受体的影响。

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Maternal Diet Supplementation with n-6/n-3 Essential Fatty Acids in a 1.2 : 1.0 Ratio Attenuates Metabolic Dysfunction in MSG-Induced Obese Mice.以1.2:1.0的比例补充n-6/n-3必需脂肪酸的母体饮食可减轻味精诱导的肥胖小鼠的代谢功能障碍。
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本文引用的文献

1
Low-Intensity swimming training after weaning improves glucose and lipid homeostasis in MSG hypothalamic obese mice.断乳后低强度游泳训练改善 MSG 下丘脑肥胖小鼠的糖脂稳态。
Endocr Res. 2011;36(2):83-90. doi: 10.3109/07435800.2010.534750.
2
Calorie restriction and endurance exercise share potent anti-inflammatory function in adipose tissues in ameliorating diet-induced obesity and insulin resistance in mice.热量限制和耐力运动在改善饮食诱导的肥胖和胰岛素抵抗方面,在脂肪组织中具有强大的抗炎功能。
Nutr Metab (Lond). 2010 Jul 16;7:59. doi: 10.1186/1743-7075-7-59.
3
Autonomic activity and glycemic homeostasis are maintained by precocious and low intensity training exercises in MSG-programmed obese mice.
早期、低强度的训练可以维持肥胖型肥胖症(MSG 肥胖症)小鼠的自主活动和血糖稳态。
Endocrine. 2009 Dec;36(3):510-7. doi: 10.1007/s12020-009-9263-2. Epub 2009 Oct 24.
4
Effects of exercise training and diet on lipid kinetics during free fatty acid-induced insulin resistance in older obese humans with impaired glucose tolerance.运动训练和饮食对糖耐量受损的老年肥胖人群在游离脂肪酸诱导的胰岛素抵抗期间脂质动力学的影响。
Am J Physiol Endocrinol Metab. 2009 Aug;297(2):E552-9. doi: 10.1152/ajpendo.00220.2009. Epub 2009 Jun 16.
5
Swimming exercise at weaning improves glycemic control and inhibits the onset of monosodium L-glutamate-obesity in mice.断奶时进行游泳锻炼可改善血糖控制,并抑制小鼠左旋谷氨酸钠诱导肥胖的发生。
J Endocrinol. 2009 Jun;201(3):351-9. doi: 10.1677/JOE-08-0312. Epub 2009 Mar 18.
6
S6K directly phosphorylates IRS-1 on Ser-270 to promote insulin resistance in response to TNF-(alpha) signaling through IKK2.S6K通过IKK2直接使胰岛素受体底物1(IRS-1)的丝氨酸270位点磷酸化,以响应肿瘤坏死因子-α(TNF-α)信号传导,从而促进胰岛素抵抗。
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