The Estrogenic Inhibition of Eating

Geary, Nori

doi:10.1007/0-306-48643-1_12

Cited by 31 publications

(58 citation statements)

References 203 publications

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“…Consistent with previous reports (22,28,31,36,39), when tested several weeks post-OVX, estradiol-treated rats ate smaller but more frequent spontaneous meals than oiltreated controls, and total daily food intake did not differ between groups. Ghrelin (6.0 nmol ip) significantly increased food intake in oil-treated OVX rats by decreasing the latency to onset of the next spontaneous meal after injection, and there was a nonsignificant decrease in the duration of the following intermeal interval, with no increase in meal size (Table 2).…”

Section: Resultssupporting

confidence: 91%

“…Then, to investigate the role of ghrelin in OVX-induced hyperphagia and weight gain, we assessed the effects of OVX on plasma ghrelin levels and hypothalamic expression of the orexigenic neuropeptides NPY (neuropeptide Y) and AgRP (Agouti-related protein), both of which have been reported to increase in male rats after ghrelin administration (3,5,9,(25)(26)(27). Finally, to investigate whether ghrelin plays a necessary role in the normal, E2-mediated ovarian inhibition of eating and body weight (22,28), we compared the effects of OVX in Ghsr Ϫ/Ϫ and wild-type mice. The collective results revealed substantial and physiologically relevant sex differences in the acute eating-stimulatory effect of ghrelin that are mediated in large part by an activational effect of E2.…”

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Estradiol-Dependent Decrease in the Orexigenic Potency of Ghrelin in Female Rats

et al. 2007

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Ghrelin, the only known orexigenic gut hormone, is secreted mainly from the stomach, increases with fasting and before meal initiation in humans and rats, and increases food intake after central or peripheral administration. To investigate sex differences in the action of ghrelin, we assessed the effects of exogenous ghrelin in intact male and female rats, the effects of exogenous ghrelin in ovariectomized (OVX) and estradiol (E2)-treated female rats, as well as the effects of OVX on plasma ghrelin and hypothalamic orexigneic neuropeptide expression in rats and on food intake and weight gain in transgenic mice lacking the ghrelin receptor (Ghsr ؊/؊ mice). Male and OVX female rats were significantly more sensitive than intact female rats to the orexigenic effects of both centrally (intra-third ventricular, i3vt, 0.01, 0.1, and 1.0 nmol) and systemically (ip, 3, 6, and 9 nmol) administered ghrelin. This difference is likely to be estradiol dependent because E2 attenuated the orexigenic action of ghrelin in OVX female and male rats. Furthermore, OVX increased food intake and body weight in wild-type mice, but not in Ghsr ؊/؊ mice, suggesting that OVX increases food intake by releasing ghrelin from a tonic inhibitory effect of estradiol. In addition, following OVX, there was an increase in plasma ghrelin that was temporally associated with increased food intake, body weight, and hypothalamic neuropeptide Y and Agoutirelated protein mRNA expression. Collectively, these data suggest that estradiol inhibits the orexigenic action of ghrelin in females, that weight gain associated with OVX is ghrelin mediated, and that this endocrine interaction may account for an important sex differences in food intake and the regulation of body weight. Diabetes 56:1051-1058, 2007 T he 28 -amino acid peptide ghrelin was discovered in 1999 (1) to be the endogenous ligand of the growth hormone secretagogue receptor (GHSR) (2). The biological functions of ghrelin have been the subject of intensive research (1,3-5). One apparent physiological role of ghrelin is in the control of eating and energy balance (1,3-7). Systemic ghrelin administration stimulates eating in rats and humans (1,5,8 -11). Additionally, when administered directly into hypothalamus (as well as other brain sites; rev. in 12), ghrelin also stimulates eating, perhaps via GHSR located in this part of the brain (13). The orexigenic action of ghrelin can be reduced by antagonism of endogenous ghrelin signaling by administration of ghrelin antibodies either peripherally or centrally (9,14,15), GHSR antagonists (16), or GHSR antisense mRNA (17). Furthermore, GHSR-null mice (Ghsr Ϫ/Ϫ mice) that are fed a high-fat diet eat less and gain less weight than control mice (18,19).An important question that has received little attention is whether there are sex differences in the orexigenic effect of ghrelin. Prominent sex differences, predominately mediated by estradiol (E2), have been reported in the effects of several other endocrine signals that alter eating, including cholecystokin...

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Section: Resultssupporting

confidence: 91%

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Estradiol-Dependent Decrease in the Orexigenic Potency of Ghrelin in Female Rats

et al. 2007

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“…Anorexia may also be a normal response to a variety of physiological or pathological conditions. An extensively studied physiological condition is the reliable and phasic decrease in food intake that follows the cyclic increase in estrogens in rodents and primates, including humans (Geary, 2004). Although several hypothalamic nuclei express estrogen receptors, it seems accepted that the ones expressed by the PVN mediate the anorectic effects of estradiol.…”

Section: Histamine-induced Loss Of Appetite Is An Adaptive Anorexia: mentioning

confidence: 99%

The Histamine H₃ Receptor and Eating Behavior

Passani¹,

Blandina²,

Torrealba³

2010

J Pharmacol Exp Ther

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Interest in the histaminergic system as a potential target for the treatment of feeding disorders is driven by the unsatisfactory history of the pharmacotherapy of obesity. Eating behavior is regulated by a complex interplay of central neurotransmitter systems, peripheral endocrine stimuli, the circadian rhythm, and environmental cues, all factors that change the behavioral state and alter homeostatic aspects of appetite and energy expenditure. Key factors driving eating behavior are appetite and satiety that are regulated through different mechanisms. Brain histamine has long been considered a satiety signal in the nervous system. Recent observations, however, indicate that histamine does not meet the criteria for being a satiety signal, because augmented histamine release accompanies the appetitive phase of feeding behavior rather than food consumption and satiety. The appetitive phase requires a high and yet optimal arousal state, and the histaminergic system is crucial for sustaining a high degree of arousal during motivated behavior. Histamine H 1 receptors in the brain are crucial for the regulation of the diurnal rhythm of food intake and the regulation of obesity; however, from a therapeutic standpoint, no brain-penetrating H 1 receptor agonists have been identified that would have antiobesity effects. Despite conflicting preclinical data, insights are emerging into the potential role of histamine H 3 receptors as a target of antiobesity therapeutics. The aim of this review is to outline the relevance of the histaminergic system in controlling feeding behavior and evaluate the potential therapeutic use of histaminergic ligands for the treatment of eating disorders.

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“…Similar mechanisms may be in operation for glucagon as the effects of glucagon and glucagon antibodies, on decreased and increased meal size, respectively, were both enhanced by estradiol in a previous study of OVX animal models (59). In the absence of estradiol, food consumption and body weight are increased (63)(64)(65). These observations are of clinical relevance as estradiol levels decrease in postmenopausal women and, notably, postmenopausal women account for a high proportion of the obese population (55).…”

Section: Discussionmentioning

confidence: 58%

Anti-climacterium effects of pomegranate concentrated solutions in ovariectomized ddY mice

Kang¹,

Choi²,

Kim³

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. In the present study, the complex anti-climacterium potential of standardized pomegranate concentrated solution (PCS) was investigated using bilateral ovariectomy (OVX) female ddY mice. Changes in body weight and gain during experimental periods, food consumption, serum estradiol levels, total body and abdominal fat densities, abdominal fat pads, and uterus weights were observed, along with the histopathology of abdominal fat pads and uterus for anti-obesity and estrogenic effects. In addition, liver weights, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, and histopathological inspections were performed to explore the hepato-protective effects. Serum total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein, and triglyceride (TG) levels were monitored for hypolipidemic effects with total body and femur mean bone mineral density (BMD), right femur wet, dry and ash weights, strength, serum osteocalcin, bone-specific alkaline phosphatase (bALP) contents, and histological and histomorphometrical analyses for anti-osteoporosis activity. As a result of OVX, notable increases in body weight and gains, food consumption, abdominal fat mass densities, weights of abdominal fat pads deposited in the abdominal cavity, and serum AST, ALT, TC, LDL, TG, and osteocalcin levels were observed, along with decreases in the uterus, liver, and femur weights, mean total body and femur BMD, femur strength, serum bALP, and estradiol levels. In addition, marked hypertrophic alterations in adipocytes located in the deposited abdominal fat pads, liver steatosis, uterine disused atrophic changes, and decreases in bone mass and structures of the femur were also observed in OVX control mice with significant increases in bone resorption markers based on histopathological and histomorphometrical analysis. However, these estrogen-deficient climacterium symptoms were significantly (P<0.05 or P<0.01) inhibited after 84 days of continuous treatment with estradiol and PCS (1, 2 and 4 ml/kg), respectively. The present results suggested that PCS was able to effectively inhibit or refine the climacterium symptoms, including obesity, hyperlipidemia, hepatic steatosis, and osteoporosis, induced by OVX in ddY mice.

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The Estrogenic Inhibition of Eating

Cited by 31 publications

References 203 publications

Estradiol-Dependent Decrease in the Orexigenic Potency of Ghrelin in Female Rats

Estradiol-Dependent Decrease in the Orexigenic Potency of Ghrelin in Female Rats

The Histamine H₃ Receptor and Eating Behavior

Anti-climacterium effects of pomegranate concentrated solutions in ovariectomized ddY mice

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The Estrogenic Inhibition of Eating

Cited by 31 publications

References 203 publications

Estradiol-Dependent Decrease in the Orexigenic Potency of Ghrelin in Female Rats

Estradiol-Dependent Decrease in the Orexigenic Potency of Ghrelin in Female Rats

The Histamine H3 Receptor and Eating Behavior

Anti-climacterium effects of pomegranate concentrated solutions in ovariectomized ddY mice

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The Histamine H₃ Receptor and Eating Behavior