{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T02:28:18Z","timestamp":1761964098439,"version":"3.32.0"},"reference-count":62,"publisher":"The Endocrine Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,9,1]]},"abstract":"<jats:p>11\u03b2-Hydroxysteroid dehydrogenase type 1 (11\u03b2-HSD1) catalyzes regeneration of active intracellular glucocorticoids in fat, liver, and discrete brain regions. Although overexpression of 11\u03b2-HSD1 in adipose tissue causes hyperphagia and the metabolic syndrome, male 11\u03b2-HSD1 null (11\u03b2-HSD1\u2212\/\u2212) mice resist metabolic disease on high-fat (HF) diet, but also show hyperphagia. This suggests 11\u03b2-HSD1 may influence the central actions of glucocorticoids on appetite and perhaps energy balance. We show that 11\u03b2-HSD1\u2212\/\u2212 mice express lower hypothalamic mRNA levels of the anorexigenic cocaine and amphetamine-regulated transcript and melanocortin-4 receptor, but higher levels of the orexigenic melanin-concentrating hormone mRNAs than controls (C57BL\/6J) on a low-fat diet (11% fat). HF (58% fat) diet promoted transient (\u223c8 wk) hyperphagia and decreased food efficiency in 11\u03b2-HSD1\u2212\/\u2212 mice and decreased melanocortin-4 receptor mRNA expression in control but not 11\u03b2-HSD1\u2212\/\u2212 mice. 11\u03b2-HSD1\u2212\/\u2212 mice showed a HF-mediated up-regulation of the orexigenic agouti-related peptide (AGRP) mRNA in the arcuate nucleus which paralleled the transient HF hyperphagia. Conversely, control mice showed a rapid (48 h) HF-mediated increase in arcuate 11\u03b2-HSD1 associated with subsequent down-regulation of AGRP. This regulatory pattern was unexpected because glucocorticoids increase AGRP, suggesting an alternate hyperphagic mechanism despite partial colocalization of 11\u03b2-HSD1 and AGRP in arcuate nucleus cells. One major alternate mechanism governing selective fat ingestion and the AGRP system is endogenous opioids. Treatment of HF-fed mice with the \u03bc opioid agonist DAMGO recapitulated the HF-induced dissociation of arcuate AGRP expression between control and 11\u03b2-HSD1\u2212\/\u2212 mice, whereas the opioid antagonist naloxone given with HF induced a rise in arcuate AGRP and blocked HF-diet induction of 11\u03b2-HSD1. These data suggest that 11\u03b2-HSD1 in brain plays a role in the adaptive restraint of excess fat intake, in part by increasing inhibitory opioid tone on AGRP expression in the arcuate nucleus.<\/jats:p>","DOI":"10.1210\/en.2006-0106","type":"journal-article","created":{"date-parts":[[2006,6,9]],"date-time":"2006-06-09T01:04:00Z","timestamp":1149815040000},"page":"4486-4495","source":"Crossref","is-referenced-by-count":40,"title":["11\u03b2-Hydroxysteroid Dehydrogenase Type 1 Induction in the Arcuate Nucleus by High-Fat Feeding: A Novel Constraint to Hyperphagia?"],"prefix":"10.1210","volume":"147","author":[{"given":"Valerie S.","family":"Densmore","sequence":"first","affiliation":[{"name":"Endocrinology Unit (V.S.D., N.M.M., J.R.S.), Queen\u2019s Medical Research Institute, Edinburgh EH16 4TJ, Scotland, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicholas M.","family":"Morton","sequence":"additional","affiliation":[{"name":"Endocrinology Unit 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