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脂联素并非小鼠运动训练诱导的葡萄糖和胰岛素耐受性改善所必需的。

Adiponectin is not required for exercise training-induced improvements in glucose and insulin tolerance in mice.

作者信息

Ritchie Ian R W, Wright David C, Dyck David J

机构信息

Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.

出版信息

Physiol Rep. 2014 Sep 11;2(9). doi: 10.14814/phy2.12146. Print 2014 Sep 1.

DOI:10.14814/phy2.12146
PMID:25214523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4270243/
Abstract

Adiponectin (Ad) is a potent insulin-sensitizing adipokine that has been found to activate pathways involved in the adaptation to exercise. Therefore, we examined whether Ad is required for the increased insulin response observed following exercise training in Ad knockout mice (AdKO). Eight weeks of exercise training significantly increased glucose and insulin tolerance in both wild type (WT) and AdKO mice. There were no differences in glucose tolerance between genotypes but insulin tolerance was improved to a greater extent in AdKO compared to WT mice following exercise training (+26%, P < 0.05). There were no genotype differences in the insulin-stimulated phosphorylation of AKT or AS160 in red or white gastrocnemius muscle (RG, WG). Exercise training increased total AKT and AS160 protein content in RG and total AS160 protein content in WG. There were no genotype differences in total AKT or AS160. However, exercise training induced a more robust increase in total AS160 in RG from AdKO (+44 ± 8%, P < 0.05) compared to WT mice (+28 ± 7%, P = 0.06). There were no differences in total GLUT4 or FAT/CD36 in RG or WG in WT or AdKO, with or without exercise training. Similarly, there were no differences in RER, VO2, or activity between any groups. Our results indicate the presence of Ad is not required for exercise-induced increases in insulin response. Furthermore, it appears that exercise may improve insulin sensitivity to a greater extent in the absence of Ad, suggesting the presence of an unknown compensatory mechanism.

摘要

脂联素(Ad)是一种强效的胰岛素增敏脂肪因子,已发现其可激活参与运动适应的信号通路。因此,我们研究了在脂联素基因敲除小鼠(AdKO)中,运动训练后观察到的胰岛素反应增强是否需要脂联素。八周的运动训练显著提高了野生型(WT)和AdKO小鼠的葡萄糖耐量和胰岛素耐量。基因型之间的葡萄糖耐量没有差异,但运动训练后,AdKO小鼠的胰岛素耐量比WT小鼠改善程度更大(提高26%,P<0.05)。在红色或白色腓肠肌(RG、WG)中,胰岛素刺激的AKT或AS160磷酸化没有基因型差异。运动训练增加了RG中总AKT和AS160蛋白含量以及WG中总AS160蛋白含量。总AKT或AS160没有基因型差异。然而,与WT小鼠(提高28±7%,P=0.06)相比,运动训练使AdKO小鼠RG中总AS160的增加更为显著(提高44±8%,P<0.05)。无论有无运动训练,WT或AdKO小鼠的RG或WG中总GLUT4或FAT/CD36均无差异。同样,任何组之间的呼吸交换率(RER)、耗氧量(VO2)或活动也没有差异。我们的结果表明,运动诱导的胰岛素反应增强不需要脂联素的存在。此外,在没有脂联素的情况下,运动似乎可以更大程度地改善胰岛素敏感性,这表明存在一种未知的代偿机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/80f37910ea75/phy2-2-e12146-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/9806055f14b0/phy2-2-e12146-g1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/baa06e7d2cb1/phy2-2-e12146-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/80f37910ea75/phy2-2-e12146-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/9806055f14b0/phy2-2-e12146-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/6e0de8472704/phy2-2-e12146-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/92e060965afe/phy2-2-e12146-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4437/4270243/24d36245d015/phy2-2-e12146-g4.jpg
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