Estradiol treatment increases feeding-induced c-Fos expression in the brains of ovariectomized rats

2001 ◽  
Vol 281 (3) ◽  
pp. R738-R746 ◽  
Author(s):  
Lisa A. Eckel ◽  
Nori Geary
Keyword(s):  
Food Intake ◽  
Neuronal Activity ◽  
Negative Feedback ◽  
Estradiol Benzoate ◽  
Brain Regions ◽  
Meal Size ◽  
Central Nucleus ◽  
Ovariectomized Rats ◽  
Estradiol Treatment ◽  
Multiple Regions

The steroid hormone estradiol decreases meal size by increasing the potency of negative-feedback signals involved in meal termination. We used c-Fos immunohistochemistry, a marker of neuronal activation, to investigate the hypothesis that estradiol modulates the processing of feeding-induced negative-feedback signals within the nucleus of the solitary tract (NTS), the first central relay of the neuronal network controlling food intake, and within other brain regions related to the control of food intake. Chow-fed, ovariectomized rats were injected subcutaneously with 10 μg 17-β estradiol benzoate or sesame oil vehicle on 2 consecutive days. Forty-eight hours after the second injections, 0, 5, or 10 ml of a familiar sweet milk diet were presented for 20 min at dark onset. Rats were perfused 100 min later, and brain tissue was collected and processed for c-Fos-like immunoreactivity. Feeding increased the number of c-Fos-positive cells in the NTS, the paraventricular nucleus of the hypothalamus (PVN), and the central nucleus of the amygdala (CeA) in oil-treated rats. Estradiol treatment further increased this response in the caudal, subpostremal, and intermediate NTS, which process negative-feedback satiation signals, but not in the rostral NTS, which processes positive-feedback gustatory signals controlling meal size. Estradiol treatment also increased feeding-induced c-Fos in the PVN and CeA. These results indicate that modest amounts of food increase neuronal activity within brain regions implicated in the control of meal size in ovariectomized rats and that estradiol treatment selectively increases this activation. They also suggest that estradiol decreases meal size by increasing feeding-related neuronal activity in multiple regions of the distributed neural network controlling meal size.

Estradiol treatment increases CCK-induced c-Fos expression in the brains of ovariectomized rats

2002 ◽  
Vol 283 (6) ◽  
pp. R1378-R1385 ◽  
Author(s):  
Lisa A. Eckel ◽  
Thomas A. Houpt ◽  
Nori Geary
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Body Weight Gain ◽  
Meal Size ◽  
Female Rats ◽  
Central Nucleus ◽  
Ovariectomized Rats ◽  
Estradiol Treatment ◽  
Central Processing ◽  
Fos Expression

The ovarian hormone estradiol reduces meal size and food intake in female rats, at least in part by increasing the satiating potency of CCK. Here we used c-Fos immunohistochemistry to determine whether estradiol increases CCK-induced neuronal activation in several brain regions implicated in the control of feeding. Because the adiposity signals leptin and insulin appear to control feeding in part by increasing the satiating potency of CCK, we also examined whether increased adiposity after ovariectomy influences estradiol's effects on CCK-induced c-Fos expression. Ovariectomized rats were injected subcutaneously with 10 μg 17β-estradiol benzoate (estradiol) or vehicle once each on Monday and Tuesday for 1 wk ( experiment 1) or for 5 wk ( experiment 2). Two days after the final injection of estradiol or vehicle, rats were injected intraperitoneally with 4 μg/kg CCK in 1 ml/kg 0.9 M NaCl or with vehicle alone. Rats were perfused 60 min later, and brain tissue was collected and processed for c-Fos immunoreactivity. CCK induced c-Fos expression in the nucleus of the solitary tract (NTS), area postrema (AP), paraventricular nucleus of the hypothalamus (PVN), and central nucleus of the amygdala (CeA) in vehicle- and estradiol-treated ovariectomized rats. Estradiol treatment further increased this response in the caudal, subpostremal, and intermediate NTS, the PVN, and the CeA, but not in the rostral NTS or AP. This action of estradiol was very similar in rats tested before ( experiment 1) and after ( experiment 2) significant body weight gain, suggesting that adiposity does not modulate CCK-induced c-Fos expression or interact with estradiol's ability to modulate CCK-induced c-Fos expression. These findings suggest that estradiol inhibits meal size and food intake by increasing the central processing of the vagal CCK satiation signal.

Food intake response to modulation of secretion of cholecystokinin in Zucker rats

1983 ◽  
Vol 244 (5) ◽  
pp. R676-R685 ◽  
Author(s):  
C. L. McLaughlin ◽  
S. R. Peikin ◽  
C. A. Baile
Keyword(s):  
Food Intake ◽  
Negative Feedback ◽  
Pancreatic Enzyme ◽  
Meal Size ◽  
Zucker Rats ◽  
Feedback Signal ◽  
Meal Frequency ◽  
Feeding Behaviors ◽  
Endogenous Release ◽  
Cck Release

Exogenous administration of cholecystokinin (CCK) decreases food intake and elicits satiety behaviors. In the present experiments, feeding behaviors of Zucker obese and lean rats were measured in response to treatments that influence endogenous secretion of CCK from the duodenum. Secretion of CCK was increased by administration of phenylalanine, a stimulant of CCK release, and of trypsin inhibitor, which binds to trypsin, a negative-feedback signal for CCK release. Both of these treatments decreased the size of the first meal after a 6-h fast and average daily meal size and increased meal frequency. Administration of trypsin, proported to decrease secretion of CCK, increased average daily meal size and decreased meal frequency. Pancrease, a pancreatic enzyme concentrate, also hypothesized to act as a negative-feedback signal for CCK release, elicited feeding behaviors similar to those of trypsin. Thus the effects of these compounds on the feeding behavior of Zucker obese and lean rats may be related to their effects on CCK secretion. The feeding behaviors of obese rats were affected less than those of lean rats by exogenous administration of CCK, but in these experiments were affected more than in lean rats by modulation of endogenous release of CCK.

Naltrexone administered to central nucleus of amygdala or PVN: neural dissociation of diet and energy

2000 ◽  
Vol 279 (1) ◽  
pp. R86-R92 ◽  
Author(s):  
Michael J. Glass ◽  
Charles J. Billington ◽  
Allen S. Levine
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Neural Circuitry ◽  
Brain Regions ◽  
Wide Distribution ◽  
Central Nucleus ◽  
Total Energy Consumption ◽  
Direct Stimulation ◽  
The Central Nervous System ◽  
Diet Intake

There is evidence that opioids may affect food consumption through mechanisms as diverse as reward or energy metabolism. However, these hypotheses are derived from studies employing peripheral or, more rarely, intracerebroventricular administration of drugs. Opioid receptors have a wide distribution in the central nervous system and include a number of regions implicated in food intake such as the hypothalamic paraventricular nucleus (PVN) and the central nucleus of the amygdala (ACe). It is not known whether local opioid receptor blockade in either of these regions will produce similar effects on food intake. To examine this issue, a chronic cannula was aimed at either the PVN or ACe of rats that were fed a choice of a high-fat and high-carbohydrate diet, which allows for the measurement of both preference and total energy consumption. Naltrexone influenced preferred and nonpreferred food consumption, depending on the site of administration. Consumption of both preferred and nonpreferred diets was suppressed after PVN naltrexone administration, whereas only preferred diet intake was reduced after ACe injection of naltrexone. The present evidence indicates that direct stimulation of different brain regions with naltrexone may be associated with diverse effects on diet selection, which may be accounted for by manipulation of specific functional neural circuitry.

Estrogen inhibition of LH and FSH secretion: effects of a GnRH antagonist

1986 ◽  
Vol 250 (4) ◽  
pp. E341-E345
Author(s):  
M. C. Charlesworth ◽  
N. B. Schwartz
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Gnrh Antagonist ◽  
Follicle Stimulating Hormone ◽  
Estradiol Benzoate ◽  
Gonadotropin Releasing Hormone ◽  
Ovariectomized Rats ◽  
Inhibitory Effects ◽  
Dependent Component ◽  
Lh Secretion

Follicle-stimulating hormone (FSH) levels are not suppressed as rapidly or to the same degree as luteinizing hormone (LH) levels in ovariectomized rats treated with either gonadotropin-releasing hormone (GnRH) antagonist or estrogen. The acute inhibitory effects of various doses of estrogen on FSH and LH secretion were examined in cannulated, 2-wk ovariectomized rats. No dose of 17 beta-estradiol, up to 2,500 ng injected intravenously, suppressed FSH, although LH secretion was inhibited 50% within 1 h by 100 ng. In another experiment, estradiol benzoate (EB; 10 or 250 micrograms; sc injection in oil) was only marginally effective in suppressing FSH, compared with LH, levels in serum. Treatment with EB 24 h before or after a 500 micrograms dose of a GnRH antagonist did not reduce LH or FSH to levels lower than those achieved with antagonist alone. These results indicate that the GnRH-dependent component of FSH release and the GnRH-independent component that is unmasked in the presence of GnRH antagonist are sensitive to negative feedback by estrogen, indicating that this steroid is not the primary inhibitory ovarian factor regulating FSH in the rat.

scholarly journals SAT-605 Characterization of Dual Projection Patterns of Refeeding-Activated Neurons in the Parasubthalamic Nucleus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Gabor Wittmann ◽  
Nicholas Cosentino ◽  
Ronald M Lechan
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Brain Regions ◽  
Central Nucleus ◽  
Free Access ◽  
Target Area ◽  
Sprague Dawley ◽  
Bed Nucleus ◽  
Alexa Fluor ◽  
The Brain

Abstract We have observed that following a fast, animals terminate their food intake within 2h after refeeding accompanied by a pattern of neuronal activation as identified by c-fos immunostaining that involves a number of brain regions associated with the regulation of food intake including the nucleus tractus solitarius (NTS), parabrachial nucleus (PBN), central nucleus of the amygdala (CEA), hypothalamic arcuate and paraventricular nuclei, and bed nucleus of the stria terminalis. We also observed striking c-fos activation in the posterior-lateral hypothalamus called the parasubthalamic nucleus or PSTN, raising the possibility that it may also be an important anorectic center in the brain. To establish how the PSTN is integrated into the CNS, we performed dual-label retrograde tract tracing studies to characterize whether refeeding-activated PSTN neurons project to one, or more than one target area in the CNS. Adult, Sprague-Dawley rats received dual stereotaxic injections of Alexa Fluor 488- and Alexa Fluor 555-conjugated cholera toxin β subunit (CTB; 0.1%, 0.5–1 µl volume) into the 1) PBN and NTS, 2) PBN and CEA and 3) NTS and CEA. After 7–12 days, the animals were fasted for 24 h and then given free access to food for 2 h before euthanasia by transcardial perfusion with 4% paraformaldehyde. Brains with successful dual injections were further processed for c-fos immunohistochemistry. The results showed that 26.5±3.8% of PSTN neurons projecting to the PBN also project to the CEA, and 34.6±7.6% of PSTN neurons that project to the CEA also project to the PBN. In addition, 20.2±2.7% of PSTN neurons that project to the PBN also project to the NTS, and 38.1±9.7% of PSTN neurons that project to the NTS also project to the PBN. Furthermore, 35.0±12.5% of PSTN neurons that project to the CEA project to the NTS and 37.1±4.0% of PSTN neurons that project to the NTS project to the CEA. Finally, up to 15% of the neurons with dual projections to the PBN and CEA contained c-fos after refeeding; up to 18% of the neurons with dual projections to the PBN and NTS contained c-fos; and up to 30% of neurons with dual projections to the NTS and CEA contained c-fos. We conclude that a large number of PSTN neurons have more than one projection site within the brain, thus the PSTN appears to have the capability of simultaneously communicating information about appetite to several, major feeding-related sites within the brain, presumably to terminate feeding.

Time course of effects of ovarian hormones on food intake and metabolism

1982 ◽  
Vol 243 (5) ◽  
pp. E407-E412 ◽  
Author(s):  
J. M. Gray ◽  
M. R. Greenwood
Keyword(s):  
Food Intake ◽  
Time Course ◽  
Body Weight Gain ◽  
Fatty Acid Synthetase ◽  
Hormone Treatment ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Treatment Groups ◽  
Adipose Tissue Lipoprotein Lipase

The effects of administration of estradiol benzoate (EB) or EB plus progesterone (EB + Prog) on feeding behavior and lipid metabolism were examined in ovariectomized rats killed 1, 2, 3, 7, or 14 days after the onset of hormone treatment. EB caused a transient decrease in food intake and body weight gain and a sustained decrease in adipose tissue lipoprotein lipase activity, and progesterone attenuated this EB effect. Hepatic acetyl CoA carboxylase (ACC) and fatty acid synthetase (FAS) activities decreased in the first days of hormone treatment (both EB and EB + Prog treatments) and returned to normal at 1 wk in both treatment groups. At 2 wk, hepatic ACC and FAS activities were greatly elevated in the EB, but not the EB + Prog group. These data demonstrate the complexity of the patterns of behavioral and metabolic responses after ovarian hormone manipulation in adult female rats.

scholarly journals Activation of Central, But Not Peripheral, Estrogen Receptors Is Necessary for Estradiol’s Anorexigenic Effect in Ovariectomized Rats

Endocrinology ◽  
2010 ◽  
Vol 151 (12) ◽  
pp. 5680-5688 ◽  
Author(s):  
Heidi M. Rivera ◽  
Lisa A. Eckel
Keyword(s):  
Food Intake ◽  
Estrogen Receptors ◽  
Estradiol Benzoate ◽  
Ovariectomized Rats ◽  
Biological Assay ◽  
Peripheral Tissues ◽  
Vaginal Cytology ◽  
Pure Antiestrogen ◽  
Anorexigenic Effect ◽  
The Brain

Estradiol appears to exert its anorexigenic effect by activating nuclear estrogen receptors (ERs), which are expressed widely in peripheral tissues and in the brain. Here, we used ICI-182,780 (ICI), a pure antiestrogen with limited ability to cross the blood-brain barrier, to assess the relative involvement of peripheral vs. central ERs to estradiol’s anorexigenic effect. Food intake was measured after peripheral (sc) administration of ICI or vehicle in ovariectomized rats treated with acute injections of estradiol benzoate and sesame oil over a 2-wk period. Uterine weight was assessed as a biological assay of peripheral ER activation. In a second experiment, food intake was measured after central (lateral ventricular) administration of ICI or vehicle in ovariectomized rats receiving acute injections of estradiol benzoate and oil over a period of 10 d. In order to assess the possible spread of ICI from the brain to the periphery, vaginal cytology samples were examined as a biological assay of peripheral ER activation. Peripherally administered ICI failed to attenuate estradiol’s anorexigenic effect at a dose that was sufficient to block estradiol’s uterotrophic effect. This suggests that peripheral activation of ERs is not necessary for estradiol’s anorexigenic effect. Although central infusion of 4 nm ICI blocked estradiol’s anorexigenic effect, it did not attenuate estradiol’s ability to increase the presence of cornified cells in vaginal cytology samples, suggesting that ICI did not leak into the periphery. We conclude that activation of central, but not peripheral, ERs is necessary for estradiol’s anorexigenic effect.

scholarly journals Hindbrain Administration of Estradiol Inhibits Feeding and Activates Estrogen Receptor-α-Expressing Cells in the Nucleus Tractus Solitarius of Ovariectomized Rats

Endocrinology ◽  
2007 ◽  
Vol 149 (4) ◽  
pp. 1609-1617 ◽  
Author(s):  
Sumpun Thammacharoen ◽  
Thomas A. Lutz ◽  
Nori Geary ◽  
Lori Asarian
Keyword(s):  
Estrogen Receptor ◽  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Estradiol Benzoate ◽  
Estrogen Receptor Α ◽  
Ovariectomized Rats ◽  
Afferent Projections ◽  
Inhibit Food Intake ◽  
17Β Estradiol ◽  
Direct Administration

17β-Estradiol (E2), acting via estrogen receptor (ER)-α, inhibits feeding in animals. One mechanism apparently involves an increase in the satiating potency of cholecystokinin (CCK) released from the small intestine by ingested food. For example, the satiating potency of intraduodenal lipid infusions is increased by E2 in ovariectomized rats; this increased satiation is dependent on CCK, and it is accompanied by increases in the numbers of ERα-positive cells that express c-Fos in a subregion of the caudal nucleus tractus solitarius (cNTS) that receives abdominal vagal afferent projections. To test whether direct administration of E2 to this area of the hindbrain is sufficient to inhibit food intake, we first implanted 0.2 μg estradiol benzoate (EB) in cholesterol or cholesterol alone either sc or onto the surface of the hindbrain over the cNTS. Food intake was significantly reduced after hindbrain EB implants but not after sc EB implants. Next we verified that equimolar hindbrain implants of E2 and EB had similar feeding-inhibitory effects and determined that only small amounts of E2 reached brain areas outside the dorsal caudal hindbrain after hindbrain implants of 3H-labeled E2. Neither plasma estradiol concentration nor plasma inflammatory cytokine concentration was increased by either hindbrain or sc EB implants. Finally, hindbrain EB implants, but not sc implants, increased c-Fos in ERα-positive cells in the cNTS after ip injection of 4 μg/kg CCK-8. We conclude that E2, acting via ERα in cNTS neurons, including neurons stimulated by ip CCK, is sufficient to inhibit feeding.

Acute activation of ERα decreases food intake, meal size, and body weight in ovariectomized rats

2007 ◽  
Vol 293 (6) ◽  
pp. R2194-R2201 ◽  
Author(s):  
Jessica Santollo ◽  
Mathew D. Wiley ◽  
Lisa A. Eckel
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Dose Range ◽  
Meal Size ◽  
Ovariectomized Rats ◽  
Acute Administration ◽  
Daily Food Intake ◽  
Ovx Rats ◽  
Daily Food ◽  
Anorexigenic Effect

Estradiol exerts many of its actions by coupling with two nuclear estrogen receptor (ER) proteins, ERα, and ERβ.While the acute, anorexigenic effect of estradiol appears to involve such a mechanism, the relative contributions of ERα and ERβ are equivocal. To address this problem, food intake was monitored in ovariectomized (OVX) rats following acute administration of a selective ERα agonist (4,4′,4′′-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol, PPT; dose range = 0–200 μg), a selective ERβ agonist (2,3-bis(4-hydroxyphenyl)-propionitrile, DPN; dose range = 0–600 μg), and a physiological (4 μg) dose of estradiol benzoate (EB). While PPT-treated rats displayed dose-dependent decreases in daily food intake and body weight, neither of these measures was influenced by any dose of DPN. In addition, DPN failed to modulate the anorexigenic effect of PPT when the two ER agonists were coadministered. Meal pattern analysis revealed that the anorexigenic effect of 75 μg PPT (a dose of PPT that produced a similar decrease in daily food intake as 4 μg EB) was mediated by a decrease in meal size, not meal number. Thus, PPT, like EB and endogenous estradiol, decreases food intake by selectively affecting the controls of meal size. The finding that acute administration of 75 μg PPT failed to induce a conditioned taste aversion suggests that the anorexigenic effect of this dose of PPT is not secondary to malaise. Taken together, our findings demonstrate that selective activation of ERα decreases food intake, body weight, and meal size in the ovariectomized rat.

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