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Endocrinology Vol. 142, No. 11 4751-4757
Copyright © 2001 by The Endocrine Society

ARTICLES

Deficits in E2-Dependent Control of Feeding, Weight Gain, and Cholecystokinin Satiation in ER-{alpha} Null Mice

Nori Geary, Lori Asarian, Kenneth S. Korach, Donald W. Pfaff and Sonoko Ogawa

Bourne Behavioral Research Laboratory, Department of Psychiatry, New York-Presbyterian Hospital-Weill Medical College of Cornell University (N.G., L.A.), White Plains, New York 10605; Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental and Health Sciences (K.S.K.), Research Triangle Park, North Carolina 27709; and Laboratory of Neurobiology and Behavior, Rockefeller University (D.K., S.O.), New York, New York 10021

Address all correspondence and requests for reprints to: Nori Geary, Ph.D., Bourne Behavioral Research Laboratory, New York-Presbyterian Hospital, 21 Bloomingdale Road, White Plains, New York 10605. E-mail: ndgeary{at}med.cornell.edu

To test the role of gene expression of the classical ER (ER{alpha}) in the inhibitory effects of E on food intake and body weight, we ovariectomized and administered E2 benzoate (75 pg/d) or vehicle to wild-type (WT) mice and mice with a null mutation of ER{alpha} ({alpha}ERKO). Mice were ovariectomized at age 9 wk, at which time there was no significant effect of genotype on food intake or body weight. During an 18-d test after recovery from ovariectomy, vehicle-treated WT mice increased daily food intake and gained more body weight than E2-treated WT mice, whereas food intake and body weight gain were not different in E2- and vehicle-treated {alpha}ERKO mice. Carcass analysis revealed parallel changes in body lipid content, but not water or protein content. Because an increase in the potency of the peripheral cholecystokinin (CCK) satiation-signaling system mediates part of E2’s influence on feeding in rats, the influence of ip injections of 250 µg of the selective CCKA receptor antagonist devazepide was then tested. Devazepide increased 3-h food intake in E2-treated WT mice, but was ineffective in both groups of {alpha}ERKO mice. Furthermore, ip injections of 4 µg/kg CCK-8 increased the number of cells expressing c-Fos immunoreactivity in the nuclei of the solitary tract of E2-treated WT mice more than it did in vehicle-treated WT mice, whereas E2 had no such effect in {alpha}ERKO mice. Thus, ER{alpha} is necessary for normal responsivity of food intake, body weight, adiposity, and the peripheral CCK satiation-signaling system to E2 in mice, and ERß is not sufficient for any of these effects. This is the first demonstration that ER{alpha} gene expression is involved in the estrogenic control of feeding behavior and weight regulation of female mice.




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