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缺氧暴露可减轻血管紧张素原酶敲除小鼠肌肉代谢、葡萄糖耐量和有氧能力的损伤。

Hypoxia exposure alleviates impaired muscular metabolism, glucose tolerance, and aerobic capacity in apelin-knockout mice.

机构信息

School of Sport Science Beijing Sport University China.

Faculty of Health, Engineering and Sciences University of Southern Queensland Toowoomba Australia.

出版信息

FEBS Open Bio. 2019 Jan 23;9(3):498-509. doi: 10.1002/2211-5463.12587. eCollection 2019 Mar.

DOI:10.1002/2211-5463.12587
PMID:30868058
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6396165/
Abstract

High altitude hypoxia adaptation can improve glucose tolerance in people with metabolic syndrome and type 2 diabetes (T2D). Apelin is an endogenous ligand of the G protein-coupled receptor APJ and has possible roles in energy metabolism. Apelin-null mice have been reported to exhibit impaired insulin sensitivity, which can be reversed by supplementation of exogenous apelin. Here, we examined the effects of 4 weeks' intermittent hypoxia exposure on physiological and biochemical variables in apelin knockout (KO) mice. Apelin KO mice exhibited decreased expression of substrate metabolism-associated genes/proteins, impaired glucose tolerance, and reduced exercise capacity compared to wild-type mice, and all of these effects were rescued by hypoxia. These findings suggest that hypoxia intervention may possibly be able to alleviate metabolic conditions caused by genetic defects.

摘要

高原低氧适应可以改善代谢综合征和 2 型糖尿病(T2D)患者的葡萄糖耐量。Apelin 是 G 蛋白偶联受体 APJ 的内源性配体,在能量代谢中可能发挥作用。已有报道称 Apelin 敲除(KO)小鼠表现出胰岛素敏感性受损,外源性 Apelin 的补充可以逆转这种情况。在这里,我们研究了 4 周间歇性低氧暴露对 Apelin KO 小鼠生理和生化变量的影响。与野生型小鼠相比,Apelin KO 小鼠表现出与底物代谢相关的基因/蛋白表达减少、葡萄糖耐量受损和运动能力降低,而这些影响都可以通过低氧来挽救。这些发现表明,低氧干预可能能够缓解由遗传缺陷引起的代谢状况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/7077a83850d6/FEB4-9-498-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/83a335c28873/FEB4-9-498-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/371b125a66a0/FEB4-9-498-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/5d0e061aeab5/FEB4-9-498-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/88b8ff49109c/FEB4-9-498-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/321f9e056c11/FEB4-9-498-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/7077a83850d6/FEB4-9-498-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/83a335c28873/FEB4-9-498-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/371b125a66a0/FEB4-9-498-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/5d0e061aeab5/FEB4-9-498-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/88b8ff49109c/FEB4-9-498-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/321f9e056c11/FEB4-9-498-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9bf/6396165/7077a83850d6/FEB4-9-498-g006.jpg

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