title: Type II corticosteroid receptor stimulation increases NPY gene expression in basomedial hypothalamus of rats.
abstract: Evidence has suggested that glucocorticoids may increase neuropeptide Y (NPY) activity and gene expression. In the present study, we sought to determine the corticosteroid receptor subtype through which glucocorticoids increase NPY gene expression in the basomedial hypothalamus. This was accomplished by continuous administration of selective type I and II corticosteroid agonists in adrenalectomized Sprague-Dawley rats. Dot-blot analysis was performed, and the amount of NPY mRNA was determined. Additionally, serum insulin and glucose concentrations were determined. Type II receptor stimulation increased NPY mRNA levels in the basomedial hypothalamus above that of sham animals. This implies that type II receptor stimulation by high physiological concentrations of serum corticosterone may also increase NPY gene expression in the basomedial hypothalamus. The type II receptor agonist-induced increase in NPY gene expression did not appear to be mediated by a decrease in serum insulin concentrations. The present results may have relevance to the increased gene expression of NPY observed in the basomedial hypothalamus of obese Zucker rats and in food-deprived animals.
authors.affiliation: Department of Foods and Nutrition, University of Georgia, Athens 30602.
authors.forename: B D
authors.initials: BD
authors.lastname: White
authors.forename: R G
authors.initials: RG
authors.lastname: Dean
authors.forename: G L
authors.initials: GL
authors.lastname: Edwards
authors.forename: R J
authors.initials: RJ
authors.lastname: Martin
mesh_terms: D000315:Adrenalectomy; D000450:Aldosterone / Q000008:administration & dosage / Q000494:pharmacology*; D000732:Androstanols / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D004347:Drug Interactions; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D007033:Hypothalamus, Middle / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D007263:Infusions, Parenteral; D007328:Insulin / Q000097:blood; D008297:Male; D015735:Mifepristone / Q000008:administration & dosage / Q000494:pharmacology; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D009478:Neuropeptide Y / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011987:Receptors, Steroid / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D013148:Spironolactone / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000732:Androstanols; D001786:Blood Glucose; D007328:Insulin; D000451:Mineralocorticoid Receptor Antagonists; D009478:Neuropeptide Y; D012333:RNA, Messenger; D011987:Receptors, Steroid; D013148:Spironolactone; D015735:Mifepristone; D000450:Aldosterone; C049154:11,17-dihydroxy-6-methyl-17-(1-propynyl)androsta-1,4,6-triene-3-one; C041006:RU 28318