Influence of ovarian hormones on development of ingestive responding to alterations in fatty acid oxidation in female rats

Women less than 50 years of age, the majority of whom are likely premenopausal and exposed to estrogen, are at greater risk of a poor short-term recovery after myocardial ischemia than men and older women. Since estrogen enhances non-cardiac lipid utilization and increased lipid utilization is associated with poor post-ischemic heart function, we determined the effect of estrogen replacement on post-ischemic myocardial function and fatty acid oxidation. Female SpragueDawley rats, either intact (n = 15) or ovariectomized and treated with 17β-estradiol (0.1 mg·kg1·day1, s.c., n = 14) or corn oil vehicle (n = 16) for 5 weeks, were compared. Function and fatty acid oxidation of isolated working hearts perfused with 1.2 mM [9,10-3H]palmitate, 5.5 mM glucose, 0.5 mM lactate, and 100 mU/L insulin were measured before and after global no-flow ischemia. Only 36% of hearts from estrogen-treated rats recovered after ischemia compared with 56% from vehicle-treated rats (p > 0.05, not significant), while 93% of hearts from intact rats recovered (p < 0.05). Relative to pre-ischemic values, post-ischemic function of estrogen-treated hearts (26.3 ± 10.1%) was significantly lower than vehicle-treated hearts (53.4 ± 11.8%, p < 0.05) and hearts from intact rats (81.9 ± 7.0%, p < 0.05). Following ischemia, fatty acid oxidation was greater in estrogen-treated hearts than in the other groups. Thus, estrogen replacement stimulates fatty acid oxidation and impairs post-ischemic recovery of isolated working hearts from ovariectomized female rats.Key words: fatty acid oxidation, estrogen, ischemia, reperfusion.

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Circulating lipids are lowered but pancreatic islet lipid metabolism and insulin secretion are unaltered in exercise-trained female rats

Applied Physiology Nutrition and Metabolism ◽

10.1139/h06-105 ◽

2007 ◽

Vol 32 (2) ◽

pp. 241-248 ◽

Cited By ~ 6

Author(s):

Julien Lamontagne ◽

Pellegrino Masiello ◽

Mariannick Marcil ◽

Viviane Delghingaro-Augusto ◽

Yan Burelle ◽

...

Keyword(s):

Fatty Acids ◽

Insulin Secretion ◽

Fatty Acid ◽

Lipid Metabolism ◽

Free Fatty Acids ◽

Fatty Acid Oxidation ◽

Female Rats ◽

Acid Oxidation ◽

Β Cell ◽

Glucose Stimulated Insulin Secretion

Deteriorating islet β-cell function is key in the progression of an impaired glucose tolerance state to overt type 2 diabetes (T2D), a transition that can be delayed by exercise. We have previously shown that trained rats are protected from heart ischemia–reperfusion injury in correlation with an increase in cardiac tissue fatty-acid oxidation. This trained metabolic phenotype, if induced in the islet, could also prevent β-cell failure in the pathogenesis of T2D. To assess the effect of training on islet lipid metabolism and insulin secretion, female Sprague–Dawley rats were exercised on a treadmill for 90 min/d, 4 d/week, for 10 weeks. Islet fatty-acid oxidation, the expression of key lipid metabolism genes, and glucose-stimulated insulin secretion were determined in freshly isolated islets from trained and sedentary control rats after a 48 h rest period from the last exercise. Although this moderate training reduced plasma glycerol, free fatty acids, and triglyceride levels by about 40%, consistent with reduced lipolysis from adipose tissue, it did not alter islet fatty-acid oxidation, nor the islet expression of key transcription factors and enzymes of lipid metabolism. The training also had no effect on glucose-stimulated insulin secretion or its amplification by free fatty acids. In summary, chronic exercise training did not cause an intrinsic change in islet lipid metabolism. Training did, however, substantially reduce the exposure of islets to exogenous lipid, thereby providing a potential mechanism by which exercise can prevent islet β-cell failure leading to T2D.

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