IMPAIRMENT OF ALBUTEROL-INDUCED SUPPRESSION OF FOOD-INTAKE IN DIABETES-MELLITUS

被引：4

作者：

BITAR, MS ^{[1
]}

KEIS, AF ^{[1
]}

OWUSU, SE ^{[1
]}

MULVEN, R ^{[1
]}

DESOUZA, EB ^{[1
]}

机构：

[1] NIDA,NEUROSCI BRANCH, NEUROBIOL LAB,BALTIMORE,MD 21224

来源：

PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR | 1992年 / 41卷 / 03期

关键词：

DIABETES; INGESTIVE BEHAVIOR; BETA-ADRENOCEPTORS; ALBUTEROL;

D O I：

10.1016/0091-3057(92)90361-I

中图分类号：

B84 [心理学]; C [社会科学总论]; Q98 [人类学];

学科分类号：

03 ; 0303 ; 030303 ; 04 ; 0402 ;

摘要：

Albuterol (salbutamol), a beta(2) adrenoreceptor agonist, produced a dose-dependent decrease in food intake in Sprague-Dawley male control rats. This phenomenon appeared to be impaired in streptozotocin (STZ) diabetic rats. The density of beta(2) adrenoreceptors in the ventromedial hypothalamic nucleus was increased as a function of diabetes. In contrast, a decrease in the ventromedial hypothalamic 5-hydroxyindoleacetic acid (5-HIAA) concentration, an indicator of serotonin (5-hydroxytryptamine; 5-HT) release or turnover rate, was observed in this disease state. Neither the beta(2) adrenoreceptor level nor 5-HT turnover rate was altered in the periventricular hypothalamic nucleus of STZ diabetic rats. The concentrations of 5-HT in both hypothalamic nuclei were unchanged in these animals. Neurochemical and behavioral abnormalities featured in the diabetic state were reversed with institution of insulin therapy. These data conclude that diabetes-related impairment in the anorexic action of albuterol may be due to derangements in ventromedial hypothalamic beta(2) adrenoreceptor function.

引用

页码：483 / 487

页数：5

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