Effects of estradiol and tamoxifen on feeding, fattiness, and some endocrine criteria in hypothalamic obese hens

In White Leghorn hens, basomedial hypothalamic (BMH) lesions result in two syndromes: a) obese, functionally castrated (OFC) hens, in which both the ventromedial hypothalamic nucleus (VMH) and the mammillary nuclei are damaged and plasma estrogen is very low; and b) obese laying (OL) hens, which hav...

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Veröffentlicht in:Pharmacology, biochemistry and behavior biochemistry and behavior, 1995, Vol.50 (1), p.55-63
Hauptverfasser: Jaccoby, S., Arnon, E., Snapir, N., Robinzon, B.
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Arnon, E.
Snapir, N.
Robinzon, B.
description In White Leghorn hens, basomedial hypothalamic (BMH) lesions result in two syndromes: a) obese, functionally castrated (OFC) hens, in which both the ventromedial hypothalamic nucleus (VMH) and the mammillary nuclei are damaged and plasma estrogen is very low; and b) obese laying (OL) hens, which have normal levels of plasma estrogen and are less obese than the former, and whose lesion is limited to the VMH. In the present study, the involvement of estrogen in regulation of fattiness and energy metabolism was assayed in OFC, OL, and control (CONT) hens. BMH lesions were made at 13 weeks of age. When the typical syndromes reached the static phase, 20 weeks later, CONT, OFC, and OL hens were divided into three subgroups and were injected for 10 weeks on each alternate day, with either 10 mg tamoxifen (TAM)/kg, 2 mg estradiol benzoate (E 2)/kg, or the vehicle, corn oil (0.5 ml). E 2 raised plasma total lipids and reduced plasma glucose, insulin, and hematocrit in all treated hens, and increased liver weight in OL and OFC, but not in CONT hens. In OFC hens only, E 2 reduced food intake (FI) and fattiness. In OL and CONT hens, E 2 increased plasma T 3, but raised the resting metabolic rate (RMR) only in CONT ones. In OFC hens, E 2 reduce plasma T 3 and T 4 without affecting RMR. E 2 reduced comb weight and egg production in CONT and more severely in OL hens. In the latter, E 2 diminished ovarian and oviduct weights, whereas in OFC hens it increased the size of the atrophied oviduct. TAM had no visible effect on OFC hens. However, in CONT and OL pullets, TAM decreased plasma total lipids, FI, liver, and ovarian and oviduct weights, abolished egg production, increased plasma glucose, insulin, T 3 and T 4, RMR, hematocrit, and comb weight, but had no effect on fattiness and body weight. It is well established that estrogen increases fattiness in cockerels and juvenile pullets. However, in adult hens in the present study, estrogen and its antagonist had no effect on fattiness in the laying ones, and even reduced body fat in the OFC hens. These results suggest that in hens, E 2 effects on fattiness alter with age. As E 2 increased plasma lipids in all hens, it may be assumed that in adult hens E 2 reduces fat deposition in depots to increase its availability for yolk production.
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In the present study, the involvement of estrogen in regulation of fattiness and energy metabolism was assayed in OFC, OL, and control (CONT) hens. BMH lesions were made at 13 weeks of age. When the typical syndromes reached the static phase, 20 weeks later, CONT, OFC, and OL hens were divided into three subgroups and were injected for 10 weeks on each alternate day, with either 10 mg tamoxifen (TAM)/kg, 2 mg estradiol benzoate (E 2)/kg, or the vehicle, corn oil (0.5 ml). E 2 raised plasma total lipids and reduced plasma glucose, insulin, and hematocrit in all treated hens, and increased liver weight in OL and OFC, but not in CONT hens. In OFC hens only, E 2 reduced food intake (FI) and fattiness. In OL and CONT hens, E 2 increased plasma T 3, but raised the resting metabolic rate (RMR) only in CONT ones. In OFC hens, E 2 reduce plasma T 3 and T 4 without affecting RMR. E 2 reduced comb weight and egg production in CONT and more severely in OL hens. In the latter, E 2 diminished ovarian and oviduct weights, whereas in OFC hens it increased the size of the atrophied oviduct. TAM had no visible effect on OFC hens. However, in CONT and OL pullets, TAM decreased plasma total lipids, FI, liver, and ovarian and oviduct weights, abolished egg production, increased plasma glucose, insulin, T 3 and T 4, RMR, hematocrit, and comb weight, but had no effect on fattiness and body weight. It is well established that estrogen increases fattiness in cockerels and juvenile pullets. However, in adult hens in the present study, estrogen and its antagonist had no effect on fattiness in the laying ones, and even reduced body fat in the OFC hens. These results suggest that in hens, E 2 effects on fattiness alter with age. 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In the present study, the involvement of estrogen in regulation of fattiness and energy metabolism was assayed in OFC, OL, and control (CONT) hens. BMH lesions were made at 13 weeks of age. When the typical syndromes reached the static phase, 20 weeks later, CONT, OFC, and OL hens were divided into three subgroups and were injected for 10 weeks on each alternate day, with either 10 mg tamoxifen (TAM)/kg, 2 mg estradiol benzoate (E 2)/kg, or the vehicle, corn oil (0.5 ml). E 2 raised plasma total lipids and reduced plasma glucose, insulin, and hematocrit in all treated hens, and increased liver weight in OL and OFC, but not in CONT hens. In OFC hens only, E 2 reduced food intake (FI) and fattiness. In OL and CONT hens, E 2 increased plasma T 3, but raised the resting metabolic rate (RMR) only in CONT ones. In OFC hens, E 2 reduce plasma T 3 and T 4 without affecting RMR. E 2 reduced comb weight and egg production in CONT and more severely in OL hens. In the latter, E 2 diminished ovarian and oviduct weights, whereas in OFC hens it increased the size of the atrophied oviduct. TAM had no visible effect on OFC hens. However, in CONT and OL pullets, TAM decreased plasma total lipids, FI, liver, and ovarian and oviduct weights, abolished egg production, increased plasma glucose, insulin, T 3 and T 4, RMR, hematocrit, and comb weight, but had no effect on fattiness and body weight. It is well established that estrogen increases fattiness in cockerels and juvenile pullets. However, in adult hens in the present study, estrogen and its antagonist had no effect on fattiness in the laying ones, and even reduced body fat in the OFC hens. These results suggest that in hens, E 2 effects on fattiness alter with age. 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and b) obese laying (OL) hens, which have normal levels of plasma estrogen and are less obese than the former, and whose lesion is limited to the VMH. In the present study, the involvement of estrogen in regulation of fattiness and energy metabolism was assayed in OFC, OL, and control (CONT) hens. BMH lesions were made at 13 weeks of age. When the typical syndromes reached the static phase, 20 weeks later, CONT, OFC, and OL hens were divided into three subgroups and were injected for 10 weeks on each alternate day, with either 10 mg tamoxifen (TAM)/kg, 2 mg estradiol benzoate (E 2)/kg, or the vehicle, corn oil (0.5 ml). E 2 raised plasma total lipids and reduced plasma glucose, insulin, and hematocrit in all treated hens, and increased liver weight in OL and OFC, but not in CONT hens. In OFC hens only, E 2 reduced food intake (FI) and fattiness. In OL and CONT hens, E 2 increased plasma T 3, but raised the resting metabolic rate (RMR) only in CONT ones. In OFC hens, E 2 reduce plasma T 3 and T 4 without affecting RMR. E 2 reduced comb weight and egg production in CONT and more severely in OL hens. In the latter, E 2 diminished ovarian and oviduct weights, whereas in OFC hens it increased the size of the atrophied oviduct. TAM had no visible effect on OFC hens. However, in CONT and OL pullets, TAM decreased plasma total lipids, FI, liver, and ovarian and oviduct weights, abolished egg production, increased plasma glucose, insulin, T 3 and T 4, RMR, hematocrit, and comb weight, but had no effect on fattiness and body weight. It is well established that estrogen increases fattiness in cockerels and juvenile pullets. However, in adult hens in the present study, estrogen and its antagonist had no effect on fattiness in the laying ones, and even reduced body fat in the OFC hens. These results suggest that in hens, E 2 effects on fattiness alter with age. As E 2 increased plasma lipids in all hens, it may be assumed that in adult hens E 2 reduces fat deposition in depots to increase its availability for yolk production.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>7700955</pmid><doi>10.1016/0091-3057(94)00251-D</doi><tpages>9</tpages></addata></record>
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subjects Aging - physiology
Animals
Antiestrogen
Biological and medical sciences
Body Composition - drug effects
Body Weight - drug effects
Chicken
Chickens
Egg laying
Energy Metabolism - drug effects
Estradiol - pharmacology
Estrogen
Estrogens - blood
Feeding Behavior - drug effects
Female
Fertility - drug effects
Functional castration
Hormones - blood
Hypothalamus - physiology
Insulin
Medical sciences
Metabolic diseases
Obesity
Organ Size - drug effects
Ovariectomy
Resting metabolic rate
Tamoxifen - pharmacology
Thyroxin
Triiodothyronine
title Effects of estradiol and tamoxifen on feeding, fattiness, and some endocrine criteria in hypothalamic obese hens
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