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热应激反应缺陷可能是代谢疾病易感性的潜在原因。

Deficiency in the Heat Stress Response Could Underlie Susceptibility to Metabolic Disease.

作者信息

Rogers Robert S, Morris E Matthew, Wheatley Joshua L, Archer Ashley E, McCoin Colin S, White Kathleen S, Wilson David R, Meers Grace M E, Koch Lauren G, Britton Steven L, Thyfault John P, Geiger Paige C

机构信息

Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS.

Department of Medicine-Gastroenterology and Hepatology, University of Missouri, Columbia, MO.

出版信息

Diabetes. 2016 Nov;65(11):3341-3351. doi: 10.2337/db16-0292. Epub 2016 Aug 23.

DOI:10.2337/db16-0292
PMID:27554472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5079638/
Abstract

Heat treatment (HT) effectively prevents insulin resistance and glucose intolerance in rats fed a high-fat diet (HFD). The positive metabolic actions of heat shock protein 72 (HSP72), which include increased oxidative capacity and enhanced mitochondrial function, underlie the protective effects of HT. The purpose of this study was to test the ability of HSP72 induction to mitigate the effects of consumption of a short-term 3-day HFD in rats selectively bred to be low-capacity runners (LCRs) and high-capacity runners (HCRs)-selective breeding that results in disparate differences in intrinsic aerobic capacity. HCR and LCR rats were fed a chow or HFD for 3 days and received a single in vivo HT (41°C, for 20 min) or sham treatment (ST). Blood, skeletal muscles, liver, and adipose tissues were harvested 24 h after HT/ST. HT decreased blood glucose levels, adipocyte size, and triglyceride accumulation in liver and muscle and restored insulin sensitivity in glycolytic muscles from LCR rats. As expected, HCR rats were protected from the HFD. Importantly, HSP72 induction was decreased in LCR rats after only 3 days of eating the HFD. Deficiency in the highly conserved stress response mediated by HSPs could underlie susceptibility to metabolic disease with low aerobic capacity.

摘要

热处理(HT)可有效预防高脂饮食(HFD)喂养大鼠的胰岛素抵抗和葡萄糖不耐受。热休克蛋白72(HSP72)的积极代谢作用,包括增加氧化能力和增强线粒体功能,是HT保护作用的基础。本研究的目的是测试诱导HSP72减轻短期3天HFD对选择性培育的低能力跑步大鼠(LCR)和高能力跑步大鼠(HCR)影响的能力——选择性育种导致内在有氧能力存在显著差异。将HCR和LCR大鼠喂食普通饲料或HFD 3天,并接受单次体内HT(41°C,20分钟)或假处理(ST)。在HT/ST后24小时采集血液、骨骼肌、肝脏和脂肪组织。HT降低了LCR大鼠的血糖水平、脂肪细胞大小以及肝脏和肌肉中的甘油三酯积累,并恢复了糖酵解肌肉中的胰岛素敏感性。正如预期那样,HCR大鼠对HFD具有抗性。重要的是,仅在食用HFD 3天后,LCR大鼠中HSP72的诱导就降低了。由HSP介导的高度保守应激反应的缺陷可能是低有氧能力个体易患代谢疾病的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/5a709b3364d6/db160292f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/6ba83466a3e0/db160292f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/f68343cd16cb/db160292f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/cfedd7e067f4/db160292f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/c724efa6356e/db160292f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/5a709b3364d6/db160292f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/6ba83466a3e0/db160292f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/f68343cd16cb/db160292f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/cfedd7e067f4/db160292f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/c724efa6356e/db160292f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/5079638/5a709b3364d6/db160292f5.jpg

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