Document Type : Original Article
Author
Endocrine and metabolism Research center,Department of Internal Medicine, Nemazee Hospital, Shiraz university of medical sciences, Shiraz, Iran
Abstract
In this article, the Effects of esreradiol on leptin and other factors as investigated. Gonadal hormones potently control food intake and body weight. In female animals, deactivation effects of estradiol acutely and chronically influence body weight homeostasis. In rats and mice, estrogen exerts a tonic inhibitory effect on meal size and daily food intake throughout the ovarian cycle and a cyclic inhibitory effect during the peri-ovulatory phase. Removal of estrogen leads to changes in meal size and duration, hyperphagia, and obesity. Estrogen has similar effects in humans where it modulates periovulatory decreases in daily food intake. Additionally, reductions in estrogen are associated with changes in body weight and fat distribution in humans, which parallel the findings in animals. Estrogen has the ability to control energy balance, food intake, and body fat distribution and this may be mediated through its interaction with orexigenic and anorexigenic hormones. This review aims to explore these interactions and discuss the link between estrogen and obesity. Differences in adipose mass and distribution and glucose homeostasis in males and females have been attributed at least partly to sex steroids. Menopause is characterized by reduced estrogen production and a shift in adipose distribution from peripheral to central accumulation. Hyper androgenization in polycystic ovarian disease is associated with central (visceral) obesity, insulin resistance, and type 2 diabetes. Moreover, ERα deficiency resulted in a decrease in energy expenditure with no change in food intake. Estrogen regulates energy balance through the central nervous system, as evidenced by the development of hyperphagia and reduced energy expenditure in response to injection of ERα RNAi into the ventromedial nucleus of the hypothalamus.
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