Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters

Availability of oxidizable metabolic fuels is a primary factor affecting fertility, in female mammals. Reductions in metabolic fuel availability caused by food deprivation, treatment with pharmacological inhibitors of glycolysis (2-deoxy-D-glucose, 2DG) and fatty acid oxidation (methyl palmoxirate,...

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Main Author: Panicker, Anitha K
Language:ENG
Published: ScholarWorks@UMass Amherst 1999
Subjects:
Online Access:https://scholarworks.umass.edu/dissertations/AAI9950197
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spelling ndltd-UMASS-oai-scholarworks.umass.edu-dissertations-32792020-12-02T14:29:28Z Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters Panicker, Anitha K Availability of oxidizable metabolic fuels is a primary factor affecting fertility, in female mammals. Reductions in metabolic fuel availability caused by food deprivation, treatment with pharmacological inhibitors of glycolysis (2-deoxy-D-glucose, 2DG) and fatty acid oxidation (methyl palmoxirate, MP) or with insulin, inhibit both estrous cyclicity and estrous behavior in Syrian hamsters. In this study, the effects of fuel deprivation on neural estrogen receptors, the pathways by which metabolic fuel status is conveyed in food deprived animals to higher forebrain circuits and the changes in estrogen receptor (ER) mRNA expression after fuel deprivation have been studied. Food deprivation or treatment with 2DG+MP decreased detectable number of estrogen receptor immunoreactive (ERIR) cells in the ventromedial hypothamic nucleus (VMH), increased the detectable number of ERIR in the arcuate nucleus (ARC) and the posterior parvicellular portion of the hypothalamic paraventricular nucleus (PaPo) without any effect on anterior parvicellular portion of the paraventricular nucleus (PaMP) and posterodorsal portion of the medial amygdala (MePD). Insulin treatment significantly reduced sexual receptivity in ovariectomized, steroid treated animals. It also resulted in similar changes in detectable number of ERIR cells in the VMH and medial preoptic area (mPOA) as that caused by food deprivation, cold exposure or treatment with metabolic inhibitors. Area postrema (AP) plays a significant role in transmitting metabolic information to the forebrain along with the nucleus of solitary tract (NTS) and the vagus nerves. The results of the present study clearly show that AP lesions prevent the suppression of estrous behavior, but not the suppression of estrous cyclicity, caused by food deprivation. AP lesions also blocked the suppression of estrous behavior in insulin treated animals. The last part of the project determined the changes in ER mRNA expression in VMH, 12 h after treatment with 2DG and MP. The results showed no differences between the ER mRNA levels between the fed and fuel deprived animals. 1999-01-01T08:00:00Z text https://scholarworks.umass.edu/dissertations/AAI9950197 Doctoral Dissertations Available from Proquest ENG ScholarWorks@UMass Amherst Neurology
collection NDLTD
language ENG
sources NDLTD
topic Neurology
spellingShingle Neurology
Panicker, Anitha K
Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters
description Availability of oxidizable metabolic fuels is a primary factor affecting fertility, in female mammals. Reductions in metabolic fuel availability caused by food deprivation, treatment with pharmacological inhibitors of glycolysis (2-deoxy-D-glucose, 2DG) and fatty acid oxidation (methyl palmoxirate, MP) or with insulin, inhibit both estrous cyclicity and estrous behavior in Syrian hamsters. In this study, the effects of fuel deprivation on neural estrogen receptors, the pathways by which metabolic fuel status is conveyed in food deprived animals to higher forebrain circuits and the changes in estrogen receptor (ER) mRNA expression after fuel deprivation have been studied. Food deprivation or treatment with 2DG+MP decreased detectable number of estrogen receptor immunoreactive (ERIR) cells in the ventromedial hypothamic nucleus (VMH), increased the detectable number of ERIR in the arcuate nucleus (ARC) and the posterior parvicellular portion of the hypothalamic paraventricular nucleus (PaPo) without any effect on anterior parvicellular portion of the paraventricular nucleus (PaMP) and posterodorsal portion of the medial amygdala (MePD). Insulin treatment significantly reduced sexual receptivity in ovariectomized, steroid treated animals. It also resulted in similar changes in detectable number of ERIR cells in the VMH and medial preoptic area (mPOA) as that caused by food deprivation, cold exposure or treatment with metabolic inhibitors. Area postrema (AP) plays a significant role in transmitting metabolic information to the forebrain along with the nucleus of solitary tract (NTS) and the vagus nerves. The results of the present study clearly show that AP lesions prevent the suppression of estrous behavior, but not the suppression of estrous cyclicity, caused by food deprivation. AP lesions also blocked the suppression of estrous behavior in insulin treated animals. The last part of the project determined the changes in ER mRNA expression in VMH, 12 h after treatment with 2DG and MP. The results showed no differences between the ER mRNA levels between the fed and fuel deprived animals.
author Panicker, Anitha K
author_facet Panicker, Anitha K
author_sort Panicker, Anitha K
title Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters
title_short Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters
title_full Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters
title_fullStr Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters
title_full_unstemmed Neural mechanisms regulating metabolic fuel deprivation-induced infertility in Syrian hamsters
title_sort neural mechanisms regulating metabolic fuel deprivation-induced infertility in syrian hamsters
publisher ScholarWorks@UMass Amherst
publishDate 1999
url https://scholarworks.umass.edu/dissertations/AAI9950197
work_keys_str_mv AT panickeranithak neuralmechanismsregulatingmetabolicfueldeprivationinducedinfertilityinsyrianhamsters
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