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Review
. 2006 Jul 29;361(1471):1251-63.
doi: 10.1098/rstb.2006.1860.

Modulation of appetite by gonadal steroid hormones

Lori Asarian  1 , Nori Geary
Affiliations
Review

Modulation of appetite by gonadal steroid hormones

Lori Asarian et al. Philos Trans R Soc Lond B Biol Sci. .

Abstract

Several sex differences in eating, their control by gonadal steroid hormones and their peripheral and central mediating mechanisms are reviewed. Adult female rats and mice as well as women eat less during the peri-ovulatory phase of the ovarian cycle (estrus in rats and mice) than other phases, an effect under the control of cyclic changes in estradiol secretion. Women also appear to eat more sweets during the luteal phase of the cycle than other phases, possibly due to simultaneous increases in estradiol and progesterone. In rats and mice, gonadectomy reveals further sex differences: orchiectomy decreases food intake by decreasing meal frequency and ovariectomy increases food intake by increasing meal size. These changes are reversed by testosterone and estradiol treatment, respectively. A variety of peripheral feedback controls of eating, including ghrelin, cholecystokinin (CCK), glucagon, hepatic fatty acid oxidation, insulin and leptin, has been shown to be estradiol-sensitive under at least some conditions and may mediate the estrogenic inhibition of eating. Of these, most progress has been made in the case of CCK. Neurons expressing estrogen receptor-alpha in the nucleus tractus solitarius of the brainstem appear to increase their sensitivity to CCK-induced vagal afferent input so as to lead to an increase in the satiating potency of CCK, and consequently decreased food intake, during the peri-ovulatory period in rats. Central serotonergic mechanisms also appear to be part of the effect of estradiol on eating. The physiological roles of other peripheral feedback controls of eating and their central mediators remain to be established.

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Figures

Figure 1
Figure 1
Schematic depicting HPG axis control of food intake in adult male and female rats and mice. In both sexes, GnRH is synthesized in the medial preoptic area and the arcuate nucleus of the hypothalamus and transported via the portal system to the anterior pituitary where it acts on the gonadotrophs to release FSH and LH, which, in turn, control the secretion of E2, P from the ovaries and T from the testes. Positive and negative feedbacks (dashed lines) between gonads, pituitary and the hypothalamus maintain normal HPG axis function. In adult males (upper panels), constant daily T release results in a constant level of daily food intake (the circadian rhythm is controlled separately). In females (lower panels), E and P are released cyclically. E, but not P, produces the cyclic variation in food intake, with a nadir during the peri-ovulatory phase of the cycle, the night of estrus. See text for details. Dashed vertical lines in middle and right panels denote 24 hour periods; open and filled columns in right panels denote light and dark phases of the 24 hour period, respectively. D1, diestrus 1; D2, diestrus 2; P, proestrus; E, estrus. *Nocturnal food intake typically less during E than other cycle days.
Figure 2
Figure 2
Schematic depicting the effects of gonadectomy and E2 or T treatment on food intake in adult male and female rats and mice. In males (upper panels), orchidectomy (ORX; medium-dash lines in centre and right panels) results in a decrease in daily food intake, and T treatment (ORX+T; short-dashed line) reverses this effect. In females (lower panels), ovariectomy (OVX; medium-dashed lines in centre and right panels) eliminates cycling and increases daily food intake, and cyclic E2 treatment (OVX+E2; short dashed line) reverses these effects. P treatment has no effect. See text for details.
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