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 Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats

1981 ◽  
Vol 240 (5) ◽  
pp. E499-E503 ◽  
Author(s):  
S. M. Schwartz ◽  
G. N. Wade
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Reduce Food Intake ◽  
Reduced Body ◽  
Adipose Tissue Lipoprotein Lipase

The effects of estradiol and progesterone on food intake, body weight, carcass adiposity, and adipose tissue lipoprotein lipase (LPL) activity were investigated in weanling female rats. Treatment with estradiol benzoate (EB) reduced body weight gain in ovariectomized (OVX) weanlings as it does in adults. However, other responses to EB were attenuated or absent in weanlings. EB treatment did not reduce food intake, carcass adiposity, or adipose tissue LPL activity. This impaired responsiveness to EB may be due to decreased levels of cytoplasmic estrogen receptors in liver and adipose tissue (but not hypothalamus) in weanlings. On the other hand, responsiveness to progesterone was adultlike in weanlings. Treatment of OVX, EB-primed weanlings with progesterone increased food intake, body weight gain, and carcass adiposity. This adultlike responsiveness to progesterone was associated with adultlike levels of adipose tissue progestin receptors. However, progesterone treatment did not increase adipose tissue LPL activity in weanlings, indicating that changes in LPL activity are not necessary for progesterone-induced obesity.

Estrogens and antiestrogens: actions and interactions with fluphenazine on food intake and body weight in rats

1993 ◽  
Vol 264 (6) ◽  
pp. R1214-R1218 ◽  
Author(s):  
J. M. Gray ◽  
S. Schrock ◽  
M. Bishop
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Ethinyl Estradiol ◽  
Body Weight Gain ◽  
Fatty Acid Synthetase ◽  
Ovariectomized Rats ◽  
Synthetase Activity ◽  
Concurrent Administration

Treatment of ovariectomized rats for 3 days with 2 micrograms estradiol benzoate (E2B), 6 micrograms ethinyl estradiol, or 1-2 mg of either of the antiestrogens nafoxidine or tamoxifen led to similar decreases in food intake, body weight gain, adipose tissue lipoprotein lipase activity, and hepatic fatty acid synthetase activity, despite their different effects on uterine growth and induction of progestin receptors in pituitary and adipose tissue. Longer-term (2 wk) treatment with tamoxifen resulted in similar transient changes in food intake and body weight gain, as did treatment with E2B. Daily administration of 50 micrograms fluphenazine (FLU) led to significant decreases in body weight, although there was no change in food intake. Concurrent administration of FLU with either E2B or tamoxifen led to additive effects on body weight and food intake change. None of the treatments had any effect on in vitro binding of [3H]tamoxifen to antiestrogen binding sites in pooled hypothalamic-preoptic area samples.

Food intake, body weight, and adiposity in female rats: actions and interactions of progestins and antiestrogens

1981 ◽  
Vol 240 (5) ◽  
pp. E474-E481 ◽  
Author(s):  
J. M. Gray ◽  
G. N. Wade
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Antiestrogenic Activity ◽  
Ovx Rats ◽  
Increase Food Intake ◽  
Series Of Experiments ◽  
Adipose Tissue Lipoprotein Lipase

A series of experiments examined the effects of two progestins, progesterone and R 5020, and two nonsteroidal antiestrogens, nafoxidine and MER-25, on body weight and composition in female rats. Both progesterone and R 5020 increased food intake, body weight, and carcass adiposity in ovariectomized (OVX) rats treated with estradiol benzoate (EB), but neither progestin had any effect on these measures in OVX rats not treated with EB. R 5020 was substantially more effective than progesterone on all end points. Nafoxidine and MER-25 mimicked the actions of estradiol and decreased adipose tissue lipoprotein lipase (LPL) activity by 75–80%. For adipose tissue LPL activity, both nafoxidine and MER-25 were full estrogen agonists and without antiestrogenic activity. Nafoxidine also mimicked the effects of EB by reducing food intake, body weight, and carcass adiposity in OVX rats. In contrast, nafoxidine antagonized the induction of cytoplasmic progestin ([3H]R 5020) binding sites by EB in parametrial adipose tissue of OVX rats. In nafoxidine-treated OVX rats, concurrent progesterone administration had no effect on adipose tissue LPL activity, but progesterone did increase food intake, body weight, and carcass fat content. Some physiological mechanisms by which gonadal steroids may act to influence eating and adiposity are discussed.

scholarly journals Fluoxetine Mimics the Anorectic Action of Estrogen and Its Regulation of Circadian Feeding in Ovariectomized Female Rats

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 849 ◽  
Author(s):  
Yuri Nishimura ◽  
Kaori Mabuchi ◽  
Natsumi Omura ◽  
Ayako Igarashi ◽  
Megumi Miura ◽  
...  
Keyword(s):  
Food Intake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Body Weight Gain ◽  
Treated Group ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Dark Phase ◽  
Light Phase ◽  
Serotonergic Neurons ◽  
Fos Expression

Our previous study demonstrated that chronic estrogen replacement in ovariectomized rats reduces food intake and augments c-Fos expression in the suprachiasmatic nucleus (SCN), specifically during the light phase. Here, we hypothesized that serotonergic neurons in the central nervous system (CNS), which have anorectic action and play a role in regulating circadian rhythm, mediate the light phase-specific anorectic action of estrogen, and that selective serotonin reuptake inhibitors (SSRIs) mimic the hypophagic action of estrogen. Female Wistar rats were ovariectomized and treated with estradiol (E2) or cholesterol by subcutaneously implanting a silicon capsule containing E2 or cholesterol. Then, half of the cholesterol-treated rats were injected with the SSRI fluoxetine (5 mg/kg) (FLX group), while the remaining rats in the cholesterol-treated group (CON group) and all those in the E2 group were injected with saline subcutaneously twice daily at the onsets of the light and dark phases. Both E2 and FLX reduced food intake during the light phase but not the dark phase, and reduced body weight gain. In addition, both E2 and FLX augmented the c-Fos expression in the SCN, specifically during the light phase. These data indicate that FLX exerts estrogen-like antiobesity and hypophagic actions by modifying circadian feeding patterns, and suggest that estrogen regulates circadian feeding rhythm via serotonergic neurons in the CNS.

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.

scholarly journals Effect of chronic infusion of olanzapine and clozapine on food intake and body weight gain in male and female rats

Life Sciences ◽  
2007 ◽  
Vol 81 (12) ◽  
pp. 1024-1030 ◽  
Author(s):  
SuJean Choi ◽  
Briana DiSilvio ◽  
JayLynn Unangst ◽  
John D. Fernstrom
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Chronic Infusion

Stimulation of food intake and weight gain in mature female rats by bovine prolactin and bovine growth hormone

1993 ◽  
Vol 264 (6) ◽  
pp. E986-E992 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
W. J. Salsgiver ◽  
J. G. Kostelc ◽  
R. J. Collier
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Mature Female ◽  
Female Rats ◽  
Bovine Growth Hormone ◽  
Female Rat ◽  
Moisture Percentage

Recombinant bovine prolactin (rbPRL) or bovine growth hormone (rbGH) was administered to mature female rats (10/treatment group) by daily subcutaneous injection for 10 days. Doses ranged from 7 to 5,000 micrograms/day (0.03-24 mg/kg body wt). Both rbPRL and rbGH increased body weight gain and food intake, but these parameters were increased at lower doses of rbPRL (7-63 micrograms/day) than rbGH (> 190 micrograms/day). Weight gain and food intake were maximally stimulated by 190 micrograms/day rbPRL, whereas maximal increased weight gain was obtained with the highest dose of rbGH (5,000 micrograms/day). Total carcass protein was increased by both hormones; however, protein as a percentage of body weight was unchanged. Similarly, neither rbPRL nor rbGH changed the percentage of carcass moisture. Percentage of body fat was increased by rbPRL but was decreased by rbGH. Weight of the gastrointestinal tract and kidneys was increased by both hormones, but increases were in proportion to body weight gain. These data confirm that ungulate prolactin is a hyperphagic agent in the female rat. In addition, they suggest that, while prolactin stimulates growth in mature female rats, this growth is probably not via a somatogenic mechanism.

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.

Modulation of pituitary responsiveness to LHRH by androgens in ovariectomized female rats

1977 ◽  
Vol 55 (2) ◽  
pp. 188-192
Author(s):  
Padmaja N. Kulkarni ◽  
Alan A. Simpson ◽  
William H. Moger
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Releasing Hormone ◽  
Daily Dose ◽  
17Β Estradiol ◽  
High Doses ◽  
Pronounced Inhibition

The effect of androgens on pituitary response to luteinizing-hormone-releasing hormone (LHRH) and their ability to modify effects of 17β-estradiol (E2) on pituitary responsiveness to LHRH were tested in ovariectomized rats maintained on a daily dose of 0.25 μg estradiol benzoate per rat for 6 d before androgen administration.Testosterone propionate (TP) (4, 40, 400, or 4000 μg per rat), administered 24 h before LHRH (500 ng per rat), had no significant effect on luteinizing hormone (LH) or follicle-stimulating hormone (FSH) response. Similar doses of dihydrotestosterone (DHT) did not significantly alter the LH response but significantly suppressed the FSH response. Even the lowest dose completely blocked the FSH response to LHRH. TP in combination with 4 or 400 μg of E2 suppressed the stimulatory effect of E2 on both LH and FSH response to LHRH in a dose-related manner. DHT and E2 in combination affected LH response inconsistently, whereas their ratio determined FSH response; there was pronounced inhibition of FSH response in rats given high doses of DHT combined with low doses of E2; DHT inhibition of FSH response in animals receiving 4 μg of DHT with 400 μg E2 was partially overcome by the stimulatory effect of E2. Our results indicate that TP and DHT affect LH and FSH response to LHRH differently. The ratio of androgen to estrogen is important in determining the response to LHRH.

scholarly journals Modulatory Effect of Fermented Papaya Extracts on Mammary Gland Hyperplasia Induced by Estrogen and Progestin in Female Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Zhenqiang You ◽  
Junying Sun ◽  
Feng Xie ◽  
Zhiqin Chen ◽  
Sheng Zhang ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Oxidative Dna Damage ◽  
Mammary Glands ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Treatment Groups ◽  
Group A

Fermented papaya extracts (FPEs) are obtained by fermentation of papaya by Aspergillus oryzae and yeasts. In this study, we investigated the protective effects of FPEs on mammary gland hyperplasia induced by estrogen and progestogen. Rats were randomly divided into 6 groups, including a control group, an FPE-alone group, a model group, and three FPE treatment groups (each receiving 30, 15, or 5 ml/kg FPEs). Severe mammary gland hyperplasia was induced upon estradiol benzoate and progestin administration. FPEs could improve the pathological features of the animal model and reduce estrogen levels in the serum. Analysis of oxidant indices revealed that FPEs could increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, decrease malondialdehyde (MDA) level in the mammary glands and serum of the animal models, and decrease the proportion of cells positive for the oxidative DNA damage marker 8-oxo-dG in the mammary glands. Additionally, estradiol benzoate and progestin altered the levels of serum biochemical compounds such as aspartate transaminase (AST), total bilirubin (TBIL), and alanine transaminase (ALT), as well as hepatic oxidant indices such as SOD, GSH-Px, MDA, and 8-oxo-2′-deoxyguanosine (8-oxo-dG). These indices reverted to normal levels upon oral administration of a high dose of FPEs. Taken together, our results indicate that FPEs can protect the mammary glands and other visceral organs from oxidative damage.

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