Document Detail


Mechanism of the neuroleptic-induced obesity in female rats.
MedLine Citation:
PMID:  9533175     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Obesity is an undesirable side effect of neuroleptics which affects 50% approximately of patients under a program of chronic administration. 2. An animal model of neuroleptic-induced obesity and hyperphagia has been developed in female rats treated chronically with sulpiride (20 mg/Kg/ip. for 21 days). However, it is unknown whether or not the hyperphagia is essential for the development of this type of obesity. 3. Sulpiride or vehicle was administered in two experimental conditions: in the first one, food was available in an amount which was three times the previous individual daily food intake; in the second one, the daily food provision was maintained at the individual daily average before starting the treatments. This way hyperphagia was prevented in half of the groups. Besides the body weight gain measurement in all the groups, the serum levels of estradiol, prolactin, glucose and lipids were assessed in the groups with unrestricted food intake. 4. Food restriction prevented the sulpiride-induced weight gain, even though the rats displayed a permanent diestrus which suggests an hyperprolactinemia-induced impairment in the balance of the reproductive hormones that may promote weight gain. However, the basal levels of estradiol were not affected by sulpiride. 5. The high density cholesterol was significantly increased by sulpiride, and the serum glucose levels were significantly decreased, however these changes were only detected during the first week of treatment. 6. The decrease in the serum glucose levels may be an early consequence of hyperinsulinemia. 7. Neuroleptic-induced obesity in rats appears to mimic energy intake, endocrine status and carbohydrate metabolism in humans under chronic neuroleptic administration. However, these rodents did not display the typical changes in blood lipids observed in human obesity.
Authors:
T Baptista; Q Contreras; L Teneud; M A Albornoz; A Acosta; X Páez; M de Quijada; A LaCruz; L Hernández
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Progress in neuro-psychopharmacology & biological psychiatry     Volume:  22     ISSN:  0278-5846     ISO Abbreviation:  Prog. Neuropsychopharmacol. Biol. Psychiatry     Publication Date:  1998 Jan 
Date Detail:
Created Date:  1998-05-26     Completed Date:  1998-05-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8211617     Medline TA:  Prog Neuropsychopharmacol Biol Psychiatry     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  187-98     Citation Subset:  IM    
Affiliation:
Department of Physiology, Medical School, Universidad de los Andes, Mérida, Venezuela.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antipsychotic Agents / pharmacology*
Blood Glucose / drug effects,  metabolism
Cholesterol / blood
Cholesterol, HDL / blood
Cholesterol, LDL / blood
Energy Intake / drug effects
Estradiol / blood
Female
Humans
Obesity / blood,  chemically induced*,  physiopathology*
Prolactin / blood
Rats
Rats, Wistar
Sulpiride / pharmacology*
Triglycerides / blood
Weight Gain / drug effects,  physiology
Chemical
Reg. No./Substance:
0/Antipsychotic Agents; 0/Blood Glucose; 0/Cholesterol, HDL; 0/Cholesterol, LDL; 0/Triglycerides; 15676-16-1/Sulpiride; 50-28-2/Estradiol; 57-88-5/Cholesterol; 9002-62-4/Prolactin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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