Elsevier

Physiology & Behavior

Volume 99, Issue 1, 12 January 2010, Pages 142-145
Physiology & Behavior

Brief communication
Effects of estradiol on food intake and meal patterns for diets that differ in flavor and fat content

https://doi.org/10.1016/j.physbeh.2009.10.009Get rights and content

Abstract

Apart from the well known inhibitory effects of estradiol on food intake, meal size, and body weight in female rats that have been documented over the past thirty years, a more recent report presents the opposite finding; that a large dose of estradiol can increase food intake and weight gain in gonadally intact female rats presented with a palatable diet. The purpose of the present experiment was to further examine this hypothesis by evaluating the ability of estradiol to influence feeding behavior in ovariectomized rats presented with diets that differ in flavor and fat content. Female rats were given a cyclic regimen of estradiol benzoate treatment (5.0 or 20.0 µg) or the oil vehicle and were presented with the standard chow diet or a diet with a higher fat content and chocolate flavor. Food intake, meal size, and meal number were monitored three days after the first injection of estradiol or oil. Compared to the chow diet, food intake increased when animals had access to the chocolate/fat diet during the vehicle treatment condition. Both doses of estradiol significantly decreased food intake, meal size, and body weight gain when animals were presented with either the standard chow diet or the chocolate/fat diet. These findings indicate that estradiol does not stimulate the intake of a palatable diet in ovariectomized rats, and suggest that previous results showing that estradiol enhanced eating and weight gain stemmed from a disruption of the hypothalamic–pituitary–gonadal axis when intact females received a large dose of exogenous estradiol.

Introduction

In addition to their effects on reproductive physiology and behavior, ovarian hormones (e.g., estradiol) also influence regulatory processes such as the control of food intake and body weight [1], [2]. For example, in a wide range of mammalian species, estradiol produces an inhibitory effect on food intake [3], [4], [5], [6], [7], an effect that is mediated in large part by a decrease in meal size [6], [8], [9]. In female rats, withdrawal of estradiol following ovariectomy causes a significant increase in food intake and meal size, and a concomitant increase in body weight compared to gonadally intact females [8], [10], [11], [12]. Treating ovariectomized rats with physiological doses of estradiol reduces food intake and body weight and restores meal patterns to those seen in intact cycling rats [8].

Apart from these well established effects of estradiol on feeding behavior and body weight, data from a more recent study suggest that estradiol has the opposite effect on food intake; namely that it increases the intake of a palatable food (chocolate cake mixture). In that experiment, a pharmacological dose of estradiol valerate (EV, 1500 µg/kg) administered to gonadally intact female rats increased the intake of the chocolate cake mixture relative to controls when animals were presented with that diet 11 days after the EV injection [13]. The effects of EV on ovarian cyclicity were not evaluated. According to the authors, the anorectic effect of estradiol reported in the studies cited above results from the use of experimental procedures that lead to neophobia and malaise following the initial exposure to estradiol, an effect that presumably gets associated with that diet [13].

The following experiment was therefore conducted to further explore the hypothesis that estradiol can increase the consumption of a palatable diet and evaluate the physiological significance of this effect. To test this hypothesis, we treated ovariectomized rats with cyclic regimens of nearly physiological and supraphysiological doses of estradiol and measured food intake and meal patterns when the animals were presented with diets that differed in flavor and fat content. Examining changes in ingestive behavior following estradiol replacement in ovariectomized rats avoids the potential confound of a disruption of the hypothalamic–pituitary–gonadal axis that can occur when intact females are treated with exogenous estradiol [14]. To minimize the potential effect of neophobia and the likelihood that females would acquire an estradiol-induced aversion to the diets that might mask an increase in food intake, animals had access to each diet for two weeks before the onset of estradiol treatment.

Section snippets

Animals, housing, and ovariectomy

Ten female Long–Evans rats (Blue Spruce) obtained from Harlan (Indianapolis, IN) served as subjects in this experiment. Animals were approximately 50 days of age upon arrival and were individually housed in stainless steel cages (18 × 18 × 23 cm) in a windowless colony room. The room was maintained at 20 ± 3 °C with a 12:12 h light–dark cycle (lights on at 0:400 h). A white noise generator (Lafayette Instruments, Lafayette, IN) was used to mask any outside noise. Pelleted rodent chow (Mazuri, Brentwood,

23-h food and water intake

The data collected during the 72 h period following the first EB or oil injection were analyzed, as this time point models behavioral estrus in the cyclic hormone replacement regimen that was used [15]. Estradiol treatment decreased intake of both diets (Fig. 1). The ANOVA revealed significant main effects of hormone (F [2, 16] = 15.96, p < 0.001) and diet type (F [1, 9] = 5.58, p < 0.05) on 23 h food intake. The hormone–diet interaction was not statistically significant (p > 0.05). Post hoc tests

Discussion

The main goal of this experiment was to determine if estradiol treatment could increase the intake of a palatable diet in female rats as has been previously reported [13]. Ovariectomized rats received a nearly physiological (5.0 µg) or supraphysiological (20.0 µg) regimen of estradiol or vehicle treatment, and food intake and meal patterns during the 72-h period following the first EB or oil injection were analyzed. In support of the hypothesis that estradiol exerts an inhibitory effect on food

Acknowledgements

This work was supported in part by NIH R15-HD053382.

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