Ovariectomized Highly Fit Rats Are Protected against Diet-Induced Insulin Resistance

被引：11

作者：

Park, Young-Min ^{[1
]}

Kanaley, Jill A. ^{[1
]}

Zidon, Terese M. ^{[1
]}

Welly, Rebecca J. ^{[1
]}

Scroggins, Rebecca J. ^{[1
]}

Britton, Steven L. ^{[2
]}

Koch, Lauren G. ^{[2
]}

Thyfault, John P. ^{[3
]}

Booth, Frank W. ^{[4
]}

Padilla, Jaume ^{[1
,5
,6
]}

Vieira-Potter, Victoria J. ^{[1
]}

机构：

[1] Univ Missouri, Nutr & Exercise Physiol, 204 Gwynn Hall, Columbia, MO 65211 USA

[2] Univ Michigan, Dept Anesthesiol, Sch Med, Ann Arbor, MI 48109 USA

[3] Univ Kansas, Med Ctr, Dept Mol Integrat Physiol, Kansas City, KS 66103 USA

[4] Univ Missouri, Biomed Sci, 204 Gwynn Hall, Columbia, MO 65211 USA

[5] Univ Missouri, Child Hlth, 204 Gwynn Hall, Columbia, MO 65211 USA

[6] Univ Missouri, Dalton Cardiovasc Res Ctr, 204 Gwynn Hall, Columbia, MO 65211 USA

来源：

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE | 2016年 / 48卷 / 07期

基金：

美国国家卫生研究院;

关键词：

ESTROGEN LOSS; OVARIECTOMY; EXERCISE; SPONTANEOUS PHYSICAL ACTIVITY; SKELETAL MUSCLE METABOLISM; ENERGY EXPENDITURE; HIGH-FAT DIET; ARTIFICIAL SELECTION; AEROBIC CAPACITY; SKELETAL-MUSCLE; INDUCED OBESITY; OXIDATIVE-PHOSPHORYLATION; CARDIOVASCULAR EVENTS; METABOLIC SYNDROME; MITOCHONDRIAL; EXERCISE;

D O I：

10.1249/MSS.0000000000000898

中图分类号：

G8 [体育];

学科分类号：

04 ; 0403 ;

摘要：

Introduction: In the absence of exercise training, rats selectively bred for high intrinsic aerobic capacity (high-capacity running (HCR)) are protected against ovariectomy (OVX)-induced insulin resistance (IR) and obesity compared with those bred for low intrinsic aerobic capacity (low-capacity running (LCR)). Purpose: This study determined whether OVX HCR rats remain protected with exposure to high-fat diet (HFD) compared with OVX LCR rats. Methods: Female HCR and LCR rats (n = 36; age, 27-33 wk) underwent OVX and were randomized to a standard chow diet (NC, 5% kcal fat) or HFD (45% kcal fat) ad libitum for 11 wk. Total energy expenditure, resting energy expenditure, spontaneous physical activity (SPA), and glucose tolerance were assessed midway, whereas fasting circulating metabolic markers, body composition, adipose tissue distribution, and skeletal muscle adenosine monophosphate-activated protein kinase (AMPK), and mitochondrial markers were assessed at sacrifice. Results: Both HCR and LCR rats experienced HFD-induced increases in total and visceral adiposity after OVX. Despite similar gains in adiposity, HCR rats were protected from HFD-induced IR and reduced total energy expenditure observed in LCR rats (P < 0.05). This metabolic protection was likely attributed to a compensatory increase in SPA and associated preservation of skeletal muscle AMPK activity in HCR; however, HFD significantly reduced SPA and AMPK activity in LCR (P < 0.05). In both lines, HFD reduced citrate synthase activity, gene expression of markers of mitochondrial biogenesis (tFAM, NRF1, and PGC-1 alpha), and protein levels of mitochondrial oxidative phosphorylation complexes I, II, IV, and V in skeletal muscle (all P < 0.05). Conclusion: After OVX, HCR and LCR rats differentially respond to HFD such that HCR increase while LCR decrease SPA. This "physical activity compensation'' likely confers protection from HFD-induced IR and reduced energy expenditure in HCR rats.

引用

页码：1259 / 1269

页数：11

共 41 条

[1]

Booth FW, 1985, J APPL PHYSIOL, V2011, P1497

[2] PGC-1α, SIRT1 and AMPK, an energy sensing network that controls energy expenditure [J].