PROGESTERONE INDUCED INSULIN RESISTANCE- AN ANIMAL STUDY
Journal Title: Journal of Evidence Based Medicine and Healthcare - Year 2019, Vol 6, Issue 11
Abstract
BACKGROUND The occurrence of gestational diabetes in pregnant nondiabetic women is one of the observations in humans pointing to an interaction between progesterone and insulin. Oral contraceptive pill containing norethister one has been shown to increase serum glucose concentration. In an era when progestational agents are widely used for contraception and for maintenance of pregnancy, it is important that we gain more knowledge about the hyperglycemicaction of progesterone and its effect on reproductive function. Objectives-Insulin resistance is an important defect in the pathogenesis of noninsulin dependent diabetes mellitus (NIDDM). Insulin resistance is accepted to be a risk factor for hypertension, dyslipidemia, atherosclerotic vascular disease, coronary artery disease & stroke. Hyperinsulinemia is consideredasa marker of insulin resistance. In patients with gestational diabetes mellitus & polycystic ovarian syndrome hyperinsulinemia stimulate ovarian androgenic hormones& these products act directly on peripheral tissues to promote insulin resistance. Effect of progesterone on gestational diabetes & polycytic ovarian syndrome, and the cellular & molecular mechanism of insulin resistance is the study of interest. MATERIALS AND METHODS Sixty female albino rats weighing around 200 gram showing regular estrous cycle were chosen. Progesterone injections were given in varying doses and for varying periods. Control animals were given only castor oil injections. Blood was collected at the end of the experimental period, blood glucose and serum insulin was estimated along with uterine glycogen content. RESULTS Blood glucose and insulin levels were found to be increased, whereas uterine glycogen content decreased according to the dosage and duration of injections. CONCLUSION Though the hyperglycemic effect of progesterone seems to be facilitatory to reproductive function, an excessive response can lead to gestational diabetes.
Authors and Affiliations
Sahila Mohamed Kunju, Fousia L
Keywords
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- EP ID EP615609
- DOI 10.18410/jebmh/2019/194
- Views 83
- Downloads 0
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