Antagonism of specific corticotropin-releasing factor receptor subtypes selectively modifies weight loss in restrained rats

Department of Foods and Nutrition, University of Georgia, Athens, Georgia Submitted 17 March 2008 ; accepted in final form 13 October 2008 Rats exposed to 3 h of restraint stress on each of 3 days (RRS) lose weight on the days of RRS and gain weight at the same rate as controls after stress ends, bu...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2008-12, Vol.295 (6), p.R1762-R1773
Hauptverfasser: Chotiwat, Christina, Harris, Ruth B. S
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container_end_page R1773
container_issue 6
container_start_page R1762
container_title American journal of physiology. Regulatory, integrative and comparative physiology
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creator Chotiwat, Christina
Harris, Ruth B. S
description Department of Foods and Nutrition, University of Georgia, Athens, Georgia Submitted 17 March 2008 ; accepted in final form 13 October 2008 Rats exposed to 3 h of restraint stress on each of 3 days (RRS) lose weight on the days of RRS and gain weight at the same rate as controls after stress ends, but do not return to the weight of controls. RRS rats also show an exaggerated endocrine response to subsequent novel stressors. Studies described here tested the effects of corticotropin-releasing factor receptor (CRFR) antagonism on RRS-induced weight loss, hypophagia, and corticosterone release during mild stress in the postrestraint period. Weight loss was not prevented by either peripheral or third-ventricle administration of a CRFR1 antagonist, antalarmin, before each restraint. Antalarmin did, however, allow recovery of body weight in the poststress period. Third-ventricle administration of a CRFR2 antagonist, antisauvagine 30, had no effect in RRS rats but caused sustained weight loss in control animals. Surprisingly, third-ventricle administration of the nonselective CRFR antagonist, astressin, caused hypophagia and reversible weight loss in control rats. It had no effect in RRS rats. None of the antagonists modified the corticosterone response to RRS or to mild stress in the post-RRS period, but antalarmin suppressed corticosterone during the period of restraint in Control rats. These results suggest that CRFR1 activation is required for the initiation of events that lead to a prolonged down-regulation of body weight in RRS rats. The sustained reduction in body weight is independent of the severity of hypophagia on the days of restraint and of RRS-induced corticosterone release. third ventricle; hypothalamic-pituitary adrenal axis; food intake; body weight Address for reprint requests and other correspondence: Ruth B. S. Harris, Dept. of Foods and Nutrition, Univ. of Georgia, Dawson Hall, Athens, GA 30605 (e-mail: harrisrb{at}uga.edu )
doi_str_mv 10.1152/ajpregu.00196.2008
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Third-ventricle administration of a CRFR2 antagonist, antisauvagine 30, had no effect in RRS rats but caused sustained weight loss in control animals. Surprisingly, third-ventricle administration of the nonselective CRFR antagonist, astressin, caused hypophagia and reversible weight loss in control rats. It had no effect in RRS rats. None of the antagonists modified the corticosterone response to RRS or to mild stress in the post-RRS period, but antalarmin suppressed corticosterone during the period of restraint in Control rats. These results suggest that CRFR1 activation is required for the initiation of events that lead to a prolonged down-regulation of body weight in RRS rats. The sustained reduction in body weight is independent of the severity of hypophagia on the days of restraint and of RRS-induced corticosterone release. third ventricle; hypothalamic-pituitary adrenal axis; food intake; body weight Address for reprint requests and other correspondence: Ruth B. S. 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S</creatorcontrib><title>Antagonism of specific corticotropin-releasing factor receptor subtypes selectively modifies weight loss in restrained rats</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>Department of Foods and Nutrition, University of Georgia, Athens, Georgia Submitted 17 March 2008 ; accepted in final form 13 October 2008 Rats exposed to 3 h of restraint stress on each of 3 days (RRS) lose weight on the days of RRS and gain weight at the same rate as controls after stress ends, but do not return to the weight of controls. RRS rats also show an exaggerated endocrine response to subsequent novel stressors. Studies described here tested the effects of corticotropin-releasing factor receptor (CRFR) antagonism on RRS-induced weight loss, hypophagia, and corticosterone release during mild stress in the postrestraint period. Weight loss was not prevented by either peripheral or third-ventricle administration of a CRFR1 antagonist, antalarmin, before each restraint. Antalarmin did, however, allow recovery of body weight in the poststress period. Third-ventricle administration of a CRFR2 antagonist, antisauvagine 30, had no effect in RRS rats but caused sustained weight loss in control animals. Surprisingly, third-ventricle administration of the nonselective CRFR antagonist, astressin, caused hypophagia and reversible weight loss in control rats. It had no effect in RRS rats. None of the antagonists modified the corticosterone response to RRS or to mild stress in the post-RRS period, but antalarmin suppressed corticosterone during the period of restraint in Control rats. These results suggest that CRFR1 activation is required for the initiation of events that lead to a prolonged down-regulation of body weight in RRS rats. The sustained reduction in body weight is independent of the severity of hypophagia on the days of restraint and of RRS-induced corticosterone release. third ventricle; hypothalamic-pituitary adrenal axis; food intake; body weight Address for reprint requests and other correspondence: Ruth B. S. 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Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chotiwat, Christina</au><au>Harris, Ruth B. S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antagonism of specific corticotropin-releasing factor receptor subtypes selectively modifies weight loss in restrained rats</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2008-12-01</date><risdate>2008</risdate><volume>295</volume><issue>6</issue><spage>R1762</spage><epage>R1773</epage><pages>R1762-R1773</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><coden>AJPRDO</coden><abstract>Department of Foods and Nutrition, University of Georgia, Athens, Georgia Submitted 17 March 2008 ; accepted in final form 13 October 2008 Rats exposed to 3 h of restraint stress on each of 3 days (RRS) lose weight on the days of RRS and gain weight at the same rate as controls after stress ends, but do not return to the weight of controls. RRS rats also show an exaggerated endocrine response to subsequent novel stressors. Studies described here tested the effects of corticotropin-releasing factor receptor (CRFR) antagonism on RRS-induced weight loss, hypophagia, and corticosterone release during mild stress in the postrestraint period. Weight loss was not prevented by either peripheral or third-ventricle administration of a CRFR1 antagonist, antalarmin, before each restraint. Antalarmin did, however, allow recovery of body weight in the poststress period. Third-ventricle administration of a CRFR2 antagonist, antisauvagine 30, had no effect in RRS rats but caused sustained weight loss in control animals. Surprisingly, third-ventricle administration of the nonselective CRFR antagonist, astressin, caused hypophagia and reversible weight loss in control rats. It had no effect in RRS rats. None of the antagonists modified the corticosterone response to RRS or to mild stress in the post-RRS period, but antalarmin suppressed corticosterone during the period of restraint in Control rats. These results suggest that CRFR1 activation is required for the initiation of events that lead to a prolonged down-regulation of body weight in RRS rats. The sustained reduction in body weight is independent of the severity of hypophagia on the days of restraint and of RRS-induced corticosterone release. third ventricle; hypothalamic-pituitary adrenal axis; food intake; body weight Address for reprint requests and other correspondence: Ruth B. S. Harris, Dept. of Foods and Nutrition, Univ. of Georgia, Dawson Hall, Athens, GA 30605 (e-mail: harrisrb{at}uga.edu )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>18922964</pmid><doi>10.1152/ajpregu.00196.2008</doi><oa>free_for_read</oa></addata></record>
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subjects Animals
Appetite, Obesity, and Digestion
Brain
Corticosterone - blood
Corticotropin-Releasing Hormone - administration & dosage
Dose-Response Relationship, Drug
Eating - drug effects
Feeding Behavior - drug effects
Hormones
Infusions, Parenteral
Injections, Subcutaneous
Male
Peptide Fragments - administration & dosage
Pituitary gland
Prosencephalon - drug effects
Prosencephalon - metabolism
Prosencephalon - physiopathology
Pyrimidines - administration & dosage
Pyrroles - administration & dosage
Rats
Rats, Sprague-Dawley
Receptors, Corticotropin-Releasing Hormone - antagonists & inhibitors
Receptors, Corticotropin-Releasing Hormone - metabolism
Restraint, Physical
Rodents
Stress, Psychological - metabolism
Stress, Psychological - physiopathology
Time Factors
Weight
Weight Loss - drug effects
title Antagonism of specific corticotropin-releasing factor receptor subtypes selectively modifies weight loss in restrained rats
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