Relative contribution of type I and II corticosterone receptors in VMH lesion-induced obesity and hyperinsulinemia
| Autor: | Terrie Thomas, R. D. Stith, Lynn D. Devenport |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Agonist
Receptors Steroid endocrine system medicine.medical_specialty Time Factors Physiology medicine.drug_class Population Stimulation Hyperphagia Biology Weight Gain Rats Sprague-Dawley chemistry.chemical_compound Corticosterone Hyperinsulinism Physiology (medical) Internal medicine medicine Hyperinsulinemia Animals Insulin Androstanols Obesity education Receptor Aldosterone education.field_of_study Adrenalectomy medicine.disease Rats Endocrinology chemistry Ventromedial Hypothalamic Nucleus Female hormones hormone substitutes and hormone antagonists Glucocorticoid medicine.drug |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 266:R1623-R1629 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.1994.266.5.r1623 |
| Popis: | Ventromedial hypothalamic (VMH) lesion-induced obesity is accompanied by hyperinsulinemia and hyperphagia, which are dependent upon corticosterone (Cort) for their expression. Whether Cort exerts these actions through its stimulation of type I or II Cort receptor populations is unknown. Therefore, food intake and weight gain were measured in obese adrenalectomized VMH-lesioned rats given continuous infusion of various doses of either a type I-receptor agonist (aldosterone), a type II-receptor agonist (RU-28362), or several combination doses. Similarly, the receptor population responsible for lesion-induced hyperinsulinemia was identified. Type II receptor stimulation restored the hyperphagia, weight gain, and hyperinsulinemia of adrenalectomized VMH-lesioned animals, while type I receptor stimulation blocked their weight loss. |
| Databáze: | OpenAIRE |
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