Modulation of insulin resistance in ovariectomized rats by endurance exercise training and estrogen replacement

Dec 9, 2008Metabolism: clinical and experimental

How endurance exercise and estrogen affect insulin resistance in rats without ovaries

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Abstract

Ovariectomy resulted in greater final body weights, visceral fat content, and serum levels of total and low-density lipoprotein cholesterol in female rats.

Estrogen deprivation led to metabolic changes resembling insulin resistance syndrome in ovariectomized (OVX) rats.
Body weights increased by 6% when subjected to exercise training and reduced by 25% with estrogen treatment.
Visceral fat content decreased by 37% with exercise training and by 51% with estrogen treatment.
Low-density lipoprotein cholesterol levels decreased by 19% with exercise and by 26% with estrogen treatment.
Exercise training alone improved whole-body glucose tolerance by 29%, with an enhancement to 51% when combined with estrogen.
Insulin-stimulated glucose transport was reduced by 29% to 44% in OVX rats compared to sham-operated controls.

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Estrogen is known to play a role in fat metabolism, but its role in carbohydrate metabolism remains controversial. We investigated alterations in carbohydrate and fat metabolism after prolonged estrogen deprivation by determining body weight, food intake, visceral fat content, serum lipids, glucose tolerance, and insulin action on glucose transport activity in isolated soleus and extensor digitorum longus muscles. In addition, effects of endurance exercise training with or without estrogen replacement on metabolic alterations occurring under estrogen deficiency were examined. Female Sprague-Dawley rats were ovariectomized (OVX) or sham-operated (SHAM). The OVX rats remained sedentary, received 5 microg of 17beta-estradiol (E(2)), performed exercise training (ET), or underwent both estrogen treatment and exercise training (E(2) + ET) for 12 weeks. Compared with SHAM, OVX animals had greater final body weights, visceral fat content, and serum levels of total and low-density lipoprotein cholesterol (P < .05). Exercise training and E(2) significantly reduced body weights (6% and 25%), visceral fat (37% and 51%), and low-density lipoprotein cholesterol level (19% and 26%). Exercise training alone improved whole-body glucose tolerance (29%), which was enhanced to the greatest extent (51%) in the ET rats that also received E(2). Insulin-stimulated glucose transport activity in OVX group was lower than that in SHAM by 29% to 44% (P < .05). Exercise training and E(2) corrected the diminished insulin action on skeletal muscle glucose transport in OVX animals, which was partly due to elevated glucose transporter-4 protein expression. These findings indicate that 12 weeks of ovariectomy caused metabolic alterations mimicking features of the insulin resistance syndrome. Furthermore, these metabolic disturbances were attenuated by ET or E(2), whereas the beneficial interactive effects of ET and E(2) on these defects were not apparent.

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Modulation of insulin resistance in ovariectomized rats by endurance exercise training and estrogen replacement

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