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Acta Physiologica 2007; Volume 190, Supplement 655
XXXIV Congress of The Spanish Society for Physiological Sciences
7/3/2007-7/7/2007
Valladolid, Spain
17B-ESTRADIOL ON INSULIN SENSITIVITY IN RATS DURING AGING. IMPLICATIONS FOR GLUT4
Abstract number: P53
Moreno1 M, Ordonez1 P, Alonso1 A, Diaz1 F, Tolivia1 J, Gonzalez1 C
1Oviedo University.School of Medicine. Department of Functional Biology. Physiology Area. Oviedo. Spain
Aims: Insulin resistance is a common feature of aging in both human and rats, which seems to be related to a loss of gonadal function, in the case of females. Indeed, it is believed that estrogen deficiency is one of the factors responsible for the glucose homeostasis worsening. In a view of this, our first purpose was to examine the role of 17b-estradiol on insulin sensitivity during aging. Moreover, the evidence suggests that this age-related impairment of insulin action appears to affect insulin-mediated physiologic processes including glucose uptake in peripheral tissues. The second aim of this study was to determine Glut4 amount in tissues which exhibited insulin stimulated glucose uptake, such as skeletal muscle and adipose tissue.
Methods: Two groups of ovariectomized rats (aged 0, 6, 12, 18 or 24 months) treated with placebo or physiological doses of 17b-estradiol were used. Euglycemic-hyperinsulinemic clamp was performed to asses insulin sensitivity. The protein study was carried out by western-blotting.
Results: Throughout the experimental period, estradiol group was more insulin sensitive than placebo one and a decrease in insulin sensitivity was observed in both groups. Likewise, Glut4 protein content in treated group decreased from 6 month in skeletal muscle and adipose tissue.
Conclusion: Taking together our results, we propose that estradiol treatment is able to minimize the deletereous effect of aging on insulin sensitivity in sex hormones absence. Conversely, clamp results cannot be justified on the basis of Glut4 results, however upstream effects have not been excluded.
To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 190, Supplement 655 :P53