Estradiol increases the anorexia associated with increased 5-HT2C receptor activation in ovariectomized rats

Rivera, Heidi M.; Santollo, Jessica; Nikonova, Larissa; Eckel, Lisa A.

doi:10.1016/j.physbeh.2011.08.018

Cited by 24 publications

(15 citation statements)

References 50 publications

(74 reference statements)

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“…The reported effects of estradiol are complex and include attenuation of ghrelin's orexigenic action (Ferrer-Lorente et al, 2009 ), inhibition of neuropeptide Y (NPY)/agouti-related peptide (AgRP) orexigenic neurons (Olofsson et al, 2009 ), potentiation of cholecystokinin-induced satiety (Asarian and Geary, 2007 ), and stimulation of pro-opiomelanocortin (POMC) anorexigenic neurons (Zhu et al, 2015 ). Estradiol-induced hypophagia may also involve hypothalamic serotonergic activation (Pelletier et al, 2007 ; Silva et al, 2010 ; Rivera et al, 2012 ; Santollo et al, 2012 ). Moreover, estrogens influence brain areas regulating mood and cognition, such as the hippocampus, increasing the availability of monoamines through reduction of monoamine oxidase expression, stimulation of tryptophan hydroxylase, and regulation of serotonin (5-HT) neuronal transport (Ren-Patterson et al, 2006 ; Kiss et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

High-Fat Feeding Improves Anxiety-Type Behavior Induced by Ovariectomy in Rats

et al. 2018

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Menopause-induced changes may include increased incidence of both depression/anxiety and obesity. We hypothesized that behavioral changes that may develop after ovarian failure could be related to neurochemical and metabolic aspects affected by this condition and that high-fat intake may influence these associations. The present study investigated in rats the effects of ovariectomy, either alone or combined with high-fat diets enriched with either lard or fish-oil, on metabolic, behavioral and monoaminergic statuses, and on gene expression of neuropeptides and receptors involved in energy balance and mood regulation. Female rats had their ovaries removed and received either standard chow (OvxC) or high-fat diets enriched with either lard (OvxL) or fish-oil (OvxF) for 8 weeks. The Sham group received only chow diet. Ovariectomy increased feed efficiency and body weight gain and impaired glucose homeostasis and serotonin-induced hypophagia, effects either maintained or even accentuated by the lard diet but counteracted by the fish diet. The OvxL group developed obesity and hyperleptinemia. Regarding components of hypothalamic serotonergic system, both ovariectomy alone or combined with the fish diet increased 5-HT2C expression while the lard diet reduced 5-HT1B mRNA. Ovariectomy increased the anxiety index, as derived from the elevated plus maze test, while both high-fat groups showed normalization of this index. In the forced swimming test, ovariectomy allied to high-lard diet, but not to fish-oil diet, reduced the latency to immobility, indicating vulnerability to a depressive-like state. Linear regression analysis showed hippocampal AgRP to be negatively associated with the anxiety index and hypothalamic AgRP to be positively associated with the latency to immobility. These AgRp gene expression associations are indicative of a beneficial involvement of this neuropeptide on both depression and anxiety measures. The present findings demonstrate metabolic, neurochemical and behavioral alterations after ovaries removal and highlight a positive effect of high-fat feeding on the anxiety-like behavior shown by ovariectomized animals. Since the polyunsaturated ômega-3 intake (fish diet), unlike the saturated fat intake (lard diet), failed to induce deleterious metabolic or neurochemical consequences, further studies are needed focusing on the potential of this dietary component as an adjuvant anxiolytic agent after menopause.

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Section: Introductionmentioning

confidence: 99%

High-Fat Feeding Improves Anxiety-Type Behavior Induced by Ovariectomy in Rats

et al. 2018

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“…Additionally, central and peripheral E2 treatment increases leptin’s anorexigenic effect in young OVX rats [43]. Finally, in young OVX rats, a 5HT2C receptor agonist increases E2’s inhibitory effect on food intake [44]. As expected, E2 treatment increased expression of CRH, POMC, Lepr and 5HT2CR mRNAs in young rats.…”

Section: Discussionmentioning

confidence: 87%

Middle-aged female rats retain sensitivity to the anorexigenic effect of exogenous estradiol

Santollo

Yao

Neal‐Perry

et al. 2012

Behavioural Brain Research

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It is well established that estradiol (E2) decreases food intake and body weight in young female rats. However, it is not clear if female rats retain responsiveness to the anorexigenic effect of E2 during middle age. Because middle-aged females exhibit reduced responsiveness to E2, manifesting as a delayed and attenuated luteinizing hormone surge, it is plausible that middle-aged rats are less responsive to the anorexigenic effect of E2. To test this we monitored food intake in ovariohysterectomized young and middle-aged rats following E2 treatment. E2 decreased food intake and body weight to a similar degree in both young and middle-aged rats. Next, we investigated whether genes that mediate the estrogenic inhibition of food intake are similarly responsive to E2 by measuring gene expression of the anorexigenic genes corticotropin-releasing hormone (CRH), proopiomelanocortin (POMC), the long form of the leptin receptor (Lepr) and serotonin 2C receptors (5HT2CR) and the orexigenic genes agouti-related peptide (AgRP), neuropeptide Y (NPY), prepromelanin-concentrating hormone (pMCH) and orexin in the hypothalamus of young and middle-aged OVX rats treated with E2. As expected, E2 increased expression of all anorexigenic genes while decreasing expression of all orexigenic genes in young rats. Although CRH, 5HT2CR, Lepr, AgRP, NPY and orexin were also sensitive to E2 treatment in middle-aged rats, POMC and pMCH expression were not influenced by E2 in middle-aged rats. These data demonstrate that young and middle-aged rats are similarly sensitive to the anorexigenic effect of E2 and that most, but not all feeding-related genes retain sensitivity to E2.

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“…Eckel et al (209) found that the eating-inhibitory effect of the 5HT agonist fenfluramine was 1) larger in intact, cycling rats during estrus than during diestrus and 2) increased by estradiol treatment in ovariectomized rats (593). In addition, they found that intraperitoneal and lateral cerebroventricular injections of meta-chlorophenylpiperazine, a selective antagonist of 5HT 2C receptors, increased eating more in estradiol-treated than control ovariectomized rats (594). Souquet and Rowland (687), however, found no difference in the effect of chronic fenfluramine treatment in estradiol-treated than control ovariectomized rats.…”

Section: Sex Differences In Central Mechanisms Controlling Eatingmentioning

confidence: 99%

“…Rivera et al (594) reported that estradiol treatment increased 5HT 2C receptor content in the dorsal one-third of the caudal brain stem (ϳ10 -14.6 mm caudal to bregma), but not in the hypothalamus, suggesting that estradiol increases 5HT signaling by increasing the numbers of 5HT 2C receptors in the caudal brain stem. It is important to determine the relationship between these neurons and the cmNTS ER␣ neurons mediating some of estradiol's eating-inhibitory and weight-regulatory effects (please see cmNTS).…”

Section: R1238 Sex Differences In the Physiology Of Eatingmentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

391

343

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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Estradiol increases the anorexia associated with increased 5-HT2C receptor activation in ovariectomized rats

Cited by 24 publications

References 50 publications

High-Fat Feeding Improves Anxiety-Type Behavior Induced by Ovariectomy in Rats

High-Fat Feeding Improves Anxiety-Type Behavior Induced by Ovariectomy in Rats

Middle-aged female rats retain sensitivity to the anorexigenic effect of exogenous estradiol

Sex differences in the physiology of eating

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