Impaired response to exercise intervention in the vasculature in metabolic syndrome.

Impaired response to exercise intervention in the vasculature in metabolic syndrome.
复制标题

DOI:
10.1177/1479164112459664
复制
发表时间:
2013-05
影响因子:
2.4
通讯作者:
Reusch JE
Reusch JE
中科院分区:
医学3区
文献类型:
--
作者:
Knaub LA;McCune S;Chicco AJ;Miller M;Moore RL;Birdsey N;Lloyd MI;Villarreal J;Keller AC;Watson PA;Reusch JE

文献摘要

参考文献

被引文献

相似文献

体力活动降低糖尿病和心血管疾病发病率和死亡率的风险;然而,运动对糖尿病血管系统的具体影响尚未得到研究。我们假设,对糖尿病和高血压大鼠进行急性、适度的运动干预将诱导线粒体生物发生和线粒体抗氧化防御,以改善血管弹性。SHHF/MCC-FACP瘦鼠(高血压组)、肥胖组(高血压组、胰岛素抵抗组)和SpragueDawley(SD)对照组大鼠在跑台上跑步8天。在SD大鼠的主动脉裂解物中,我们观察到氧化磷酸化(OxPhos)复合体I-III的亚单位蛋白显著增加,而瘦小或肥胖的SHHF大鼠没有变化。运动还增加了SHHF瘦大鼠线粒体抗氧化防御解偶联蛋白3(UCP3)的表达(p<0.05),而运动对SD或SHHF肥胖大鼠的影响不明显。我们评估了线粒体生物发生的上游信号通路,只有过氧化物酶体增殖物激活的受体γ辅活化子1α(PGC-1α)在运动后显著降低。在这些实验中,我们证明了在慢性血管疾病模型中,运动暴露缺乏线粒体诱导。这些发现表明,慢性血管应激导致血管系统对通常由运动诱导的适应性线粒体反应的敏感性降低。
Physical activity decreases risk for diabetes and cardiovascular disease morbidity and mortality; however, the specific impact of exercise on the diabetic vasculature is unexamined. We hypothesized that an acute, moderate exercise intervention in diabetic and hypertensive rats would induce mitochondrial biogenesis and mitochondrial antioxidant defence to improve vascular resilience. SHHF/Mcc-facp lean (hypertensive) and obese (hypertensive, insulin resistant), as well as Sprague Dawley (SD) control rats were run on a treadmill for 8 days. In aortic lysates from SD rats, we observed a significant increase in subunit proteins from oxidative phosphorylation (OxPhos) complexes I–III, with no changes in the lean or obese SHHF rats. Exercise also increased the expression of mitochondrial antioxidant defence uncoupling protein 3 (UCP3) (p < 0.05) in SHHF lean rats, whereas no changes were observed in the SD or SHHF obese rats with exercise. We evaluated upstream signalling pathways for mitochondrial biogenesis, and only peroxisome proliferators–activated receptor gamma coactivator 1α (PGC-1α) significantly decreased in SHHF lean rats (p < 0.05) with exercise. In these experiments, we demonstrate absent mitochondrial induction with exercise exposure in models of chronic vascular disease. These findings suggest that chronic vascular stress results in decreased sensitivity of vasculature to the adaptive mitochondrial responses normally induced by exercise.
DOI: 10.1152/ajpheart.01279.2010
发表时间: 2011-10-01
影响因子: 4.8
作者:
Cacicedo, Jose M.;Gauthier, Marie-Soleil;Ido, Yasuo
通讯作者: Ido, Yasuo
DOI: 10.1074/jbc.m304103200
发表时间: 2003-12-19
影响因子: 4.8
作者:
Krönke, G;Bochkov, VN;Leitinger, N
通讯作者: Leitinger, N
DOI: 10.1152/ajpcell.00164.2011
发表时间: 2012-01-01
影响因子: 5.5
作者:
Du, Jianhai;Teng, Ru-Jeng;Shi, Yang
通讯作者: Shi, Yang
DOI: 10.1128/mcb.02477-05
发表时间: 2006-07-01
影响因子: 5.3
作者:
Garat, Chrystelle V.;Fankell, Dana;Klemm, Dwight J.
通讯作者: Klemm, Dwight J.
DOI: 10.1002/jnr.21317
发表时间: 2007-06-01
影响因子: 4.2
作者:
Luo, Chun Xia;Jiang, Jun;Zhu, Dong Ya
通讯作者: Zhu, Dong Ya