Estradiol and Indirect Controls of Meal Size
A plausible hypothesis is that estradiol influences food intake indirectly via its peripheral metabolic actions. Estradiol and progesterone affect the availability of circulating metabolic substrate by directing long-chain fatty acids into or out of storage in the adipose tissue. This action might influence afferents that are sensitive to metabolic flux (hypothesized to exist in the liver or central nervous system). Nevertheless, extensive tests of estradiol-treated and untreated oophorectomized rats have failed to produce direct support for this theory.[28,29,30]
Both basal plasma insulin and OB protein (leptin) are thought to be endocrine feedback signals that relate level of food intake to adipose tissue mass. Thus, another possible explanation of estradiol's effects on eating is that it influences the secretion of or sensitivity to these hormones.
There are numerous points of contact that may mediate interactions between OB protein and estradiol. For example, in both rats and humans, the ovary expresses functional leptin receptors, and estradiol apparently upregulates adipocyte OB protein production. Furthermore, basal plasma OB concentration (ng/mL/kg body fat) is greatest in premenopausal women (1.2±0.1ng/mL/kg fat mass), less in postmenopausal women (0.9±0.1ng/mL/kg), and lowest in men (0.4±0.1ng/mL/kg).
Plasma OB protein levels also increase during the luteal phase, although the significance of this increase with regard to the decrease in food intake during the periovulatory period is unclear. Finally, as with estradiol, changes in OB protein selectively affect meal size in rodents. This is the case both in genetically obese rodents that fail to produce biologically active OB protein or lack functional OB receptors as well as in normal rats receiving chronic OB protein treatment.[37,38]
Medscape General Medicine. 1998;1(3) © 1998
Cite this: The Effect of Estrogen on Appetite - Medscape - Nov 19, 1998.