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

Ahdieh, Harry; Wade, George N.

doi:10.1037/0735-7036.96.6.886

Cited by 41 publications

(26 citation statements)

References 38 publications

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“…In rodents, activity decreases within 1-9 days of ovariectomy, and estrogen treatment increases activity to postovariectomy levels within 1-12 days of treatment initiation (3,23,32,67). The similar time course of estrogen action suggests that the increase Fig.…”

Section: E762 Estrogen Decreases Body Weight In Monkeysmentioning

confidence: 71%

Selective estrogen receptor modulator promotes weight loss in ovariectomized female rhesus monkeys (Macaca mulatta) by decreasing food intake and increasing activity

Sullivan

Shearin

Koegler

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Sullivan EL, Shearin J, Koegler FH, Cameron JL. Selective estrogen receptor modulator promotes weight loss in ovariectomized female rhesus monkeys (Macaca mulatta) by decreasing food intake and increasing activity. Am J Physiol Endocrinol Metab 302: E759 -E767, 2012. First published January 17, 2012; doi:10.1152/ajpendo.00327.2011.-The effect of hormone replacement therapy (HRT) on body weight in postmenopausal women is controversial, with studies reporting an increase, a decrease, and no change in body weight. To examine estrogen receptor actions on body weight, we investigated the effects of treatment with a selective estrogen receptor modulator (SERM) on body weight, food intake, and activity and metabolic rate in a nonhuman primate model. Eighteen ovariectomized female rhesus monkeys were treated with a nonsteroidal SERM (GSK232802A, 5 mg/kg po) for 3 mo. GSK232802A decreased lutenizing hormone (P Ͻ 0.0001) and follicle-stimulating hormone levels (P Ͻ 0.0001), consistent with the estrogenic action of the compound. GSK232802A treatment produced a small but sustained weight loss (4.6 Ϯ 1.0%, P Ͻ 0.0001) and reduced adiposity (P Ͻ 0.0001), which was due at least in part to a suppression of food intake (3.6 Ϯ 3.7%, P Ͻ 0.0001). Physical activity increased during the 3rd mo of treatment (P ϭ 0.04). Baseline activity level and the change in activity due to treatment were correlated, with the most sedentary individuals exhibiting increased physical activity during the 1st mo of treatment (P ϭ 0.02). Metabolic rate did not change (P ϭ 0.58). These results indicate that GSK232802A treatment reduces body weight and adiposity in ovariectomized nonhuman primates by suppressing food intake and increasing activity, particularly in the most sedentary individuals. These findings suggest that SERM treatment may counteract weight gain in postmenopausal women.hormone replacement therapy; obesity; menopause; body fat WOMEN GAIN WEIGHT IN ADULTHOOD during the menopausal transition (16,31,45,50,53,56). However, it is unclear whether weight gain is due to age-related changes in metabolism and lifestyle, such as eating more or exercising less, or due to the decrease in ovarian hormones that occurs with menopause. The effects of hormone replacement therapy (HRT) on the body weights of postmenopausal women are controversial. Many women believe that HRT increases body weight, and 18% of hormone replacement users report weight gain as the main reason for discontinuing HRT (63,78). However, the idea that HRT increases body weight is supported by only a few studies (5, 36). The majority of studies report either that postmenopausal women on HRT have lower body weight than nonusers (82, 83) or that HRT decreases (28, 29, 47) or does not affect postmenopausal weight gain (10,84,86,91), and a few studies report that HRT causes weight loss (20). The controversy around the effects of HRT on body weight in postmenopausal women may be related in part to differing effects of the various HRT regimens that are in common use, including differences i...

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Section: E762 Estrogen Decreases Body Weight In Monkeysmentioning

confidence: 71%

Selective estrogen receptor modulator promotes weight loss in ovariectomized female rhesus monkeys (Macaca mulatta) by decreasing food intake and increasing activity

Sullivan

Shearin

Koegler

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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“…Decades of research have revealed that estrogen and its downstream target, estrogen receptor α (ERα, encoded by ESR1), are important mediators of body weight homeostasis (1)(2)(3). Multiple studies have demonstrated that activation of ERα by estrogen regulates food consumption, energy expenditure, and fat distribution (4)(5)(6).…”

Section: Estrogen Receptor α and Body Weight Homeostasismentioning

confidence: 99%

Hypoactivity following perturbed estrogen signaling in the medial amygdala

Li¹,

Krashes²

2015

J. Clin. Invest.

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C o m m e n t a r y2 5 Estrogen receptor α and body weight homeostasisDecades of research have revealed that estrogen and its downstream target, estrogen receptor α (ERα, encoded by ESR1), are important mediators of body weight homeostasis (1-3). Multiple studies have demonstrated that activation of ERα by estrogen regulates food consumption, energy expenditure, and fat distribution (4-6). Importantly, these substantial alterations in energy balance are governed by neural mechanisms, as loss of ERα expression in the CNS impairs multiple facets of homeostatic equilibrium (7). Compared with control animals, mice with a CNS-specific ERα deficiency display increased body weight, adiposity, and visceral fat distribution as the result of hyperphagia, as well as decreased heat production and physical activity. Previous studies have aimed to anatomically pinpoint and dissect specific functions of ERα in distinct regions of the brain. Deletion of Esr1 in steroidogenic factor-1 (SF1) neurons of the ventromedial hypothalamic nucleus (VMH) increases weight gain in female mice due to decreased energy expenditure through a reduction of resting metabolic rate and thermogenesis but no differences in physical activity or energy intake (7). A model in which specific regions of the brain mediate the anabolic effects of ERα are further supported by the demonstration that deletion of Esr1 from pro-opiomelanocortin (POMC) neurons of the arcuate nucleus of the hypothalamus (ARC) produces weight gain in female mice due to chronic hyperphagia (7). Regulation of food intake has been attributed to ERα expression in the preoptic anterior hypothalamus (POAH) (8), the dorsal raphe nucleus (DRN) (9), and the nucleus of the solitary tract (NTS) (10) of the hindbrain. While ERα expression in specific neurons and brain regions account for changes in heat production and food intake, the ERα-expressing neurons that alter physical activity have yet to be elucidated. In this issue, Xu et al. demonstrate that targeted deletion of Ers1 from single-minded-1 (SIM1) neurons, which are abundantly expressed in the medial amygdala (MeA), causes hypoactivity and obesity in both male and female mice (11). Metabolic consequences of ERα deficiency in SIM1 neuronsXu et al. explored potential areas of the brain that coexpress ERα and the transcription factor SIM1 by systematically quantifying overlap, and they deduced that the most abundant SIM1-expressing ERα neurons are located in the MeA (~80%) in both males and females (11). Interestingly, the number of SIM1-expressing ERα neurons in the MeA was higher in males (~7,000) compared with females (~4,000), a discrepancy that may account for disparate phenotypes between sexes. Although ERα-expressing SIM1 neurons were found in the paraventricular hypothalamic nucleus (PVN) and POAH, colocalization of SIM1 and ERα was minimal in these regions, compared with the MeA.Having located the anatomical sites of intersectional SIM1 and ERα expression, Xu and colleagues selectively deleted Esr1 from SIM1-expressing neurons (S...

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“…Ovariectomy induces an increase in food intake and decreases ambulatory and wheel running activities in rodents, all of which are reversed with estrogen replacement (Ahdieh and Wade, 1982, Colvin and Sawyer, 1969, Shimomura et al, 1990, Asarian and Geary, 2002. In fact, hypo-estrogenic states are associated with decreased activity and an increase in body weight in (Czaja and Goy, 1975, Butera and Czaja, 1984, Czaja, 1984, McCaffrey and Czaja, 1989, Jones et al, 2000, Asarian and Geary, 2002, Qiu et al, 2006b, Clegg et al, 2006, Clegg et al, 2007.…”

Section: Effects Of 17β -Estradiol On Vmh and Arcuate Neurons: Role Imentioning

confidence: 99%

“…In fact, hypo-estrogenic states are associated with decreased activity and an increase in body weight in (Czaja and Goy, 1975, Butera and Czaja, 1984, Czaja, 1984, McCaffrey and Czaja, 1989, Jones et al, 2000, Asarian and Geary, 2002, Qiu et al, 2006b, Clegg et al, 2006, Clegg et al, 2007. The anorectic effects of estrogen are thought to be mediated through CNS actions based on the findings that direct injections of E2 into the paraventricular nucleus of the hypothalamus (PVH) or arcuate/ ventromedial nucleus are effective to reduce food intake, body weight and increase wheel running activity in females (Colvin and Sawyer, 1969, Ahdieh and Wade, 1982, Butera and Czaja, 1984. It is evident that neurons in these hypothalamic nuclei regulate energy homeostasis and are affected by E2.…”

Section: Effects Of 17β -Estradiol On Vmh and Arcuate Neurons: Role Imentioning

confidence: 99%

Membrane-initiated estrogen signaling in hypothalamic neurons

Kelly

Rønnekleiv

2008

Molecular and Cellular Endocrinology

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SummaryIt is well known that many of the actions of 17β-estradiol (E2) in the central nervous system are mediated via intracellular receptor/transcription factors that interact with steroid response elements on target genes. However, there is compelling evidence for membrane steroid receptors for estrogen in hypothalamic and other brain neurons. But it is not well understood how estrogen signals via membrane receptors, and how these signals impact not only membrane excitability but also gene transcription in neurons. Indeed, it has been known for sometime that E2 can rapidly alter neuronal activity within seconds, indicating that some cellular effects can occur via membrane delimited events. In addition, E2 can affect second messenger systems including calcium mobilization and a plethora of kinases to alter cell signaling. Therefore, this review will consider our current knowledge of rapid membrane-initiated and intracellular signaling by E2 in the hypothalamus, the nature of receptors involved and how they contribute to homeostatic functions. KeywordsERα; ERβ; GPCR (G protein-coupled receptor); mER (membrane estrogen receptor that is a GPCR) Electrophysiological studies in the 1960's and 1970's suggested that gonadal steroids could directly modulate the electrical activity of hypothalamic neurons

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

Cited by 41 publications

References 38 publications

Selective estrogen receptor modulator promotes weight loss in ovariectomized female rhesus monkeys (Macaca mulatta) by decreasing food intake and increasing activity

Selective estrogen receptor modulator promotes weight loss in ovariectomized female rhesus monkeys (Macaca mulatta) by decreasing food intake and increasing activity

Hypoactivity following perturbed estrogen signaling in the medial amygdala

Membrane-initiated estrogen signaling in hypothalamic neurons

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