Independent effects of estradiol on water and food intake.

Conducted 6 experiments to examine the effects of estradiol on ingestive behaviors of guinea pigs. Estradiol treatment was found to reduce water intake independently of its actions on food intake and body weight. In the 1st experiment, minimum intake and body weight of 17 intact female guinea pigs coincided with rupture of the vaginal membrane, the estimated time of ovulation. In Exp II, injections of 3 μg of estradiol benzoate (EB)/day to 7 ovariectomized females significantly depressed food intake, water intake, and body weight, compared with 7 Ss that received oil injections. Reducing food rations to 30% below ad lib levels in Exp III by itself had no significant effect on drinking in ovariectomized Ss. In Exp IV, therefore, ovariectomized females were first placed on a food ration 30% below ad lib levels and then injected daily with either 3 μg of EB or oil. Compared with oil injections, these EB injections significantly reduced water intake, while food intake did not decline significantly. Findings indicate that estradiol operates through different mechanisms to affect water intake and food intake. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Some effects of ovarian hormones on food intake and body weight in female rats.

Conducted 3 experiments with a total of 63 ovariectomized and 41 ovariectomized-adrenalectomized Sprague-Dawley rats in which ovarian steroids affected food intake and body weight. These effects were probably mediated by estradiol and progesterone, since these 2 hormones were more effective than their principal metabolites (estrone 5a-pregnane-3,20-dione, 5ai0regnane-3,20-dione, respectively) in altering the food intake and body weight of ovariectomized Ss. Estradiol seemed to affect food intake by lowering the set point about which body weight is regulated in a dose-dependent fashion. These actions of estradiol could be attenuated or completely blocked by concurrent injections of progesterone. Estradiol-treated ovariectomized Ss were far more responsive to the weight- and appetite-promoting actions of progesterone than were ovariectomized-adrenalectomized Ss, suggesting that the principal action of progesterone on energy balance may be to interfere with the effects of estradiol. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thyroxine treatment reduces the anorectic effect of estradiol in rats.

Examined a possible interaction between thyroxine and estradiol in the control of feeding in female Sprague-Dawley rats. 14 ovariectomized Ss were given daily injections of 9.8 μg/100 g of body weight of 1-thyroxine (TX). Another 14 Ss received 0.15 ml of saline (SAL) subcutaneously each day, and food intake was measured for both groups daily. After 15 days of treatment, 8 Ss from each group were also given a single injection of 6 μg of estradiol benzoate (EB), and the remaining 6 Ss of each group received peanut oil vehicle. It was found that TX-treated Ss showed a significantly smaller drop in food intake after EB than did SAL-treated Ss. This TX-induced decrease in responsiveness to EB may be related to effects of TX on general metabolism. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Estrus- and ovariectomy-induced body weight changes: Evidence for two estrogenic mechanisms.

Estrogenic modulation of body weight in female rats is usually thought to result indirectly from estrogenic modulation of food intake. However, present data from 5 experiments with 79 female albino rats suggest that estrogens influence body weight by at least 2 mechanisms, 1 of which is independent of changes in food intake. When Ss were ovariectomized (Ovx) and food intake was limited to preoperative levels, Ovx Ss nonetheless gained large amounts of body weight. Although Ovx Ss gained more weight than controls on the same amount of food, during 33 hrs of food deprivation Ovx and control Ss lost weight at the same rate, indicating that the prefasting metabolic rates of the 2 groups were similar. During the 1st 40 days after surgery, the ano-nasal lengths of Ovx Ss increased twice as fast as that of intact Ss, which suggests a mechanism for the gradual increase in weight induced by Ovx. The weights of intact Ss followed a regular 4-day cycle during ad lib feeding, but when the estrus-associated decrease in food intake was prevented, the cyclic weight changes were altered. Thus estrogens appear to regulate body weight by modulation of food intake and modulation of ano-nasal growth or other metabolic processes. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effectiveness of estradiol in preventing and reversing obesity induced by ovariectomy and high-caloric diet in female rats.

Four experiments with 77 female Holtzman rats examined the effects of estradiol benzoate (EB) on food intake, body weight (BW), ano-nasal length, and BW/body length ratio in ovariectomized (OVX) and intact Ss maintained on control or high-fat diets and of OVX and intact Ss that had been reduced by deprivation. EB was highly effective in preventing the increase in food intake, BW, and ano-nasal growth after OVX; it was relatively ineffective in reversing BW gain after OVX. However, when ano-nasal length was also considered, BW was effective in returning OVX Ss to an appropriate BW for their increased ano-nasal length. Intact Ss fed a high-caloric diet did not exhibit an increased rate of ano-nasal growth, which indicates that the skeletal growth that occurred after OVX was not simply a result of increased food intake. It is concluded that EB modulates food intake and BW by multiple mechanisms, one of which is by modulating skeletal growth. The nature of the effect of EB on BW of intact Ss suggests that this effect occurs by still another mechanism. (13 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of hysterectomy on sexual receptivity, food intake, running wheel activity, and hypothalamic estrogen and progestin receptors in rats.

Ovariectomized-hysterectomized (OH) CD rats given sequential treatments with 2 μg of estradiol benzoate (EB) and .5 mg of progesterone (P) showed significantly higher lordosis quotients than ovariectomized (OV) Ss in 2 tests, 1 and 2 wks after surgery. To test whether the effects of hysterectomy persist, 3 groups of OV and OH Ss received weekly injections of EB, EB?+?P, or sesame oil for 4 wks, were given 2 μg of EB followed 24 hrs later by .5 mg of P, and tested for receptivity. Only the OH Ss that had received hormones for 4 wks showed a significantly higher lordosis score than OV Ss. The effects of hysterectomy on food intake, weight gain, and running wheel activity were also tested. After 1 wk of 2 μg/day EB, OH Ss lost significantly more weight and consumed less food than OV Ss, but by 2 wks the effects of hysterectomy were no longer evident. Treatment with .5 μg/day EB resulted in a significant loss in weight and food intake in OH Ss throughout the experiment. OH Ss implanted with Silastic capsules containing EB were significantly more active in running wheels than OV Ss over the 1st 9 days, but by Day 23 the activity of both groups was similar. 24 hrs following a single injection of EB, hypothalamic-preoptic area cell nuclear estrogen receptors and cytoplasmic progestin receptors were significantly higher in OH than in OV Ss. Possible mechanisms by which hysterectomy might act to enhance hormone-dependent behaviors are discussed. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Food intake, body weight, and adiposity in female rats: actions and interactions of progestins and antiestrogens

A series of experiments examined the effects of two progestins, progesterone and R 5020, and two nonsteroidal antiestrogens, nafoxidine and MER-25, on body weight and composition in female rats. Both progesterone and R 5020 increased food intake, body weight, and carcass adiposity in ovariectomized (OVX) rats treated with estradiol benzoate (EB), but neither progestin had any effect on these measures in OVX rats not treated with EB. R 5020 was substantially more effective than progesterone on all end points. Nafoxidine and MER-25 mimicked the actions of estradiol and decreased adipose tissue lipoprotein lipase (LPL) activity by 75-80%. For adipose tissue LPL activity, both nafoxidine and MER-25 were full estrogen agonists and without antiestrogenic activity. Nafoxidine also mimicked the effects of EB by reducing food intake, body weight, and carcass adiposity in OVX rats. In contrast, nafoxidine antagonized the induction of cytoplasmic progestin ([3H]R 5020) binding sites by EB in parametrial adipose tissue of OVX rats. In nafoxidine-treated OVX rats, concurrent progesterone administration had no effect on adipose tissue LPL activity, but progesterone did increase food intake, body weight, and carcass fat content. Some physiological mechanisms by which gonadal steroids may act to influence eating and adiposity are discussed.     

Dietary self-selection in intact, ovariectomized, and estradiol-treated female rats.

Six experiments with 84 Long-Evans rats investigated the effects of estrogenic stimulation on diet selection in intact estrous-cycling Ss, ovariectomized (OVX) Ss, and OVX Ss given estradiol benzoate (EB) hormone replacement therapy. In Exp I, OVX was associated with the nearly exclusive choice of the more calorically dense of a pair of diets varying in the concentration of fat, carbohydrate (COH), and protein, an effect that was decreased by EB. In Exp II, dietary self-selection was examined in intact estrous-cycling Ss given access to an isocaloric diet triplet of fat, COH, and protein. Total caloric intake and body weight did not vary across the estrous cycle. However, fat intake increased; COH and, to a lesser extent, protein intake decreased. An opposite diet selection occurred during diestrus. In Exp III, OVX resulted in progressive increases in COH and protein intake, with a concurrent decrease in fat consumption. EB partially reversed this diet selection profile (Exp IV). Results were confirmed by diet pairs with both naturally occurring and experimentally produced estrogenic stimulation (Exps V and VI). Data are consistent with previous findings showing estrogenic reduction in COH intake with standard high-COH commercial diets. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Endocrine interactions in regulation of body weight by female rats.

Studied food intakes and body weights in 65 overweight female Sprague-Dawley rats that were sham-operated, adrenalectomized, or adrenalectomized and ovariectomized. Before surgery the groups were equivalent. Postoperatively, the adrenalectomized Ss showed diminished food consumption and body weight relative to the ovariectomized and adrenalectomized Ss. Data are discussed in terms of a delicate estrogen-progesterone balance in the control of body weight. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Decrease in food intake following cortical spreading depression in static obese rats with ventromedial hypothalamic lesions.

Subjected 19 male and 23 female rats with ventromedial hypothalamic (VMH) lesions or with sham lesions to cortical spreading depression (CSD) 150 days after lesioning. Lesioned Ss showed a significantly lower food intake (as percentage of intake before CSD) than sham-lesioned Ss in the 14 days after CSD, but water intake did not differ between lesioned and sham-lesioned Ss. Both groups showed a slight decline in body weight, but lesioned Ss lost significantly more weight than sham-lesioned Ss. After 14 days, body weight, food intake, and water intake had returned to pre-CSD levels in both groups. Findings indicate that Ss with VMH damage are more sensitive to the effects of CSD than are normals and suggest that CSD acts to increase the activity of the VMH and to inhibit food intake, and this increase in activity is prolonged in VMH-lesioned Ss. (22 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lesions of the amygdala, preoptic area, and hypothalamus on estradiol-induced activity in the female rat.

In the 1st of 2 experiments, lesions of the anterior hypothalamic nucleus and the medial preoptic area sharply attenuated enhancement of wheel running by estradiol benzoate (EB) in ovariectomized albino Holtzman rats. 71 Ss received either 3.0 μg EB or oil in daily sc injections. Lesions of the corticomedial amygdala had no effect on wheel running. The hormonal effects on activity were largely independent of any changes in body weight. Exp I indicated that the anterior hypothalamic and medial preoptic areas are critically involved in the induction of activity by estradiol. However, this experiment provided no support for suggestions that the corticomedial amygdala inhibits those structures that mediate the estrogenic induction of activity. In Exp II, food deprivation was used to stimulate activity. Results suggest that the reduction in the ability of estradiol to induce activity following anterior hypothalamic and medial preoptic lesions does not reflect a general inability to become more active. (23 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Feeding, activity, and body temperature following 6-hydroxydopamine lesions in diabetes (db/db) mice.

Reductions in central catecholamines produced by intraventricular injections of 6-hydroxydopamine (6-OHDA) cause weight loss and decreased plasma glucose in diabetes (db/db) mice. The present study examined the effects of this treatment in short-term (64-day) and long-term (120-day) survival groups of female diabetes (C57 BL/KsJ-db/db) and lean mice. Phenotypically heterozygotes (db/m) and homozygotes (m/m) were used as controls. Diabetes Ss treated with 6-OHDA decreased food intake, lost weight, and maintained a lower weight than vehicle-treated controls until vehicle-treated Ss began to enter the terminal stages of the syndrome, indicated by a loss of body weight. Diabetes Ss given 6-OHDA lost weight despite reduced body temperatures and activity levels. Blood glucose levels were always lower in 6-OHDA than in ad lib fed vehicle-treated db/db Ss. The 6-OHDA treatment also improved pancreatic islet granulation. Pair feeding vehicle-treated with 6-OHDA-treated db/db Ss did not halt weight gain in the vehicle-treated group. However, measurement of carcass fat indicated similar losses in db/db-6-OHDA Ss and vehicle-treated Ss when the vehicle group was pair-fed with lean controls. Treatment with 6-OHDA produced long-term improvement in the diabetes syndrome, but the decreased body weight of the 6-OHDA-treated diabetes Ss could not be completely accounted for by changes in food intake or energy expenditure. (43 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Withdrawal of [corrected] estrogen increases hypothalamic neuropeptide Y (NPY) mRNA expression in ovariectomized obese rat

We determined the changes in neuropeptide Y (NPY) mRNA expression of the arcuate nucleus (ARC) in sham-operated (SHAM) and bilaterally ovariectomized (OVX) rats with estradiol (E2) supplement. Ovariectomy increases body weight gain for 3 weeks, accompanied by an increase of daily food intake. Ovariectomy significantly reduced serum corticosterone levels. E2 supplement reversed the effects of ovariectomy on body weight gain, food intake and serum corticosterone levels. Ovariectomy significantly increased NPY mRNA expression in the ARC. E2 supplement decreased NPY mRNA expression in the ARC of OVX rats. The present findings indicated that hypothalamic NPY mRNA expression, which involves the regulation of feeding behavior, are in parallel with circulating estrogen levels. Hypothalamic NPY mRNA expression may be important in the induction of hyperphagia after the withdrawal of estrogen by bilateral ovariectomy.     

Effects of estradiol benzoate and MER-25 on ethanol consumption in the ovariectomized rat.

Administered daily injections of estradiol benzoate (EB) to ovariectomized Wistar rats given continuous access to a 10% ethanol solution, water, and laboratory chow in 3 experiments with 78 Ss. EB led to decreases in ethanol consumption. The suppression was transient; ethanol consumption returned to the level of oil-treated controls after 14 days despite continued hormone administration. This pattern of change in ethanol consumption closely resembled previously reported effects of EB on food intake. It is proposed that a common mechanism is responsible for EB-induced suppression of both food and ethanol intake. Ethamoxytriphetol, MER-25, which antagonizes many estrogen-dependent effects but which mimics the action of EB on food intake, also led to decreases in ethanol consumption that paralleled those reported for food intake. It is suggested that voluntary consumption of ethanol by the rat is largely due to its caloric content. The relevance of these results for reports of decreased ethanol intake during pregnancy is discussed. (42 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gastric pathology and aphagia following lateral hypothalamic lesions in rats: Effects of preoperative weight reduction.

Conducted 2 experiments with a total of 105 male albino rats. In Exp I, body weights of Ss were reduced gradually to 80% of normal weight by restricting food intake (dieting), and then Ss were given lateral hypothalamic (LH) lesions. Compared with Ss of normal body weight sustaining similar brain lesions, the dieted group displayed a shorter period of postoperative aphagia and less gastric pathology. In Exp II, a group of Ss was reduced to 80% of normal body weight by withholding all food (fasting) and then given LH lesions. Compared with dieted Ss sustaining similar brain damage, the fasted group displayed a longer period of postoperative aphagia and greater gastric pathology. Since the duration of aphagia could be shortened or lengthened by simple manipulations of preoperative body weight, the adequacy of sensorimotor or motivational hypotheses to account for aphagia is questioned. Results are more consistent with the suggestion that gastric abnormalities produced by LH lesions inhibit eating. (60 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of interscapular Brown adipose tissue denervation on body weight and energy metabolism in ovariectomized and estradiol-treated rats.

Ovariectomy-induced increases and estradiol-induced decreases in body weight cannot be fully accounted for by changes in energy intake and appear to reflect alterations in thermogenesis. Because changes in energy expenditure have been linked to altered sympathetic nervous system (SNS) activity in brown adipose tissue (BAT), the role of estradiol in thermogenesis and body weight, as mediated by the SNS innervation of interscapular BAT (IBAT), was examined. In 2 experiments, with 66 Sprague-Dawley rats, the IBAT of ovariectomized Ss was bilaterally or unilaterally surgically denervated. The chow-fed, bilaterally denervated group gained more weight than the unilaterally denervated or sham-operated group, an effect that was exaggerated by sucrose feeding. Food intake did not differ among the groups within each dietary condition. Estradiol benzoate (EB; [4 μg/day, sc]) decreased body weight in all groups. Bilateral, and to a lesser extent, unilateral IBAT denervation blocked the EB-induced increase in thermogenesis. EB increased IBAT wet weight regardless of surgical treatment. The EB-induced increase in denervated IBAT wet weight was most likely due to decreased lipolysis produced by the surgical sympathectomy. Results are discussed in terms of the role of the SNS and IBAT in the mediation of estradiol-induced changes in body weight and energy metabolism. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Suckling behavior and intake control in the developing rat pup.

Studied the behavioral development of suckling and intake control in 2 experiments with Charles River CD strain rat pups. Ss were observed at the initiation, during the course, and at the termination of suckling from their anesthetized mothers. Diet was delivered intraorally through a fine tongue cannula which enabled control of timing and volume. The control of diet intake and the behavior at termination of suckling showed correlated changes from 5 to 20 days of age. When deprived of suckling (and food and water) for 8 hr, 5- and 10-day-old Ss consumed large volumes of diet (10% of body weight or greater) and terminated suckling only in the presence of extreme gastrointestinal filling. These Ss were immediately lethargic and slept after intake termination. Five-day-old Ss persisted in reattaching to the nipple when manually stimulated; 10-day-old Ss eventually refused to reattach. In contrast, 20-day-old Ss consumed more moderate volumes of diet (5% of body weight). These Ss also remained awake for a period after feeding and engaged in the exploratory and grooming activities characteristic of adult rats at the termination of feeding. These observations demonstrate major changes in suckling behavior during development. They suggest that intake control processes shift from indirect to direct and become more effective and specifically food intake related in older pups. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Development of obesity in diabetic mice pair-fed with lean siblings.

Investigated the role of hyperphagia in the obesity of the diabetic mouse, C57BL/6J/db/db. Ingestion patterns and the amount of food for 25 diabetic mice were controlled by yoking their food intake to that of 16 nonobese siblings obtaining their food by barpressing. Over a period of 6 wks, young (initial ages were 28 days) pair-fed diabetic Ss accumulated 42% more body weight and approximately 5 times more extractable carcass lipid than did their siblings. Weight gain and absolute levels of carcass fat were reduced in food-restricted diabetic Ss compared with db Ss on unrestricted food intake. However, carcass fat as percentage of wet carcass weight was virtually identical in the restricted and unrestricted db rats (47.6 vs 49.6%). From these results it is concluded that the heightened adiposity of the diabetic mouse does not require hyperphagia for its expression and thus represents a metabolic obesity. (34 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gustation and ingestive behavior in the rat.

Studied the contribution of taste to the quantitative control of intake and body weight in 15 male Wistar rats. Gustatory deafferentation was produced by combined bilateral section of the chorda tympani and glossopharyngeal nerves and the pharyngeal branch of the vagus nerve. The procedure did not affect the condition of the mouth, impair orientation to sensory stimuli, or severely disrupt the consummatory sequence. Nevertheless, deafferented Ss showed reduced responsiveness to food and water, elevated quinine HCl aversion thresholds, and impaired feeding efficiency. Food and water intake and body weight remained below control levels for at least 40–50 days postoperatively. Food intake deficits were not observed when Ss were offered ad lib pablum, a result suggesting that increased palatability could compensate for decreased gustatory input. The order of recovery of food intake through different diet types suggests a heightened responsiveness to taste stimuli. The effects of gustatory deafferentation are compared with those seen after section of trigeminal orosensory nerves, and the differential contributions of oral taste and oral touch are discussed. (42 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of ovariectomy on meal pattern in the albino rat.

In a study with 24 female albino Sherman rats, it was found that after ovariectomy most Ss increased food intake while continuing to eat discrete meals. Meal size increased in ovariectomized Ss, whereas meal frequency decreased. It is suggested that ovariectomy impairs the onset of satiety during a meal but not the ability to regulate total intake through modification of intermeal interval. (21 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)