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pubmed-article:15241725pubmed:abstractTextFollowing extensive suprasellar operations for excision of hypothalamic tumors, some patients develop morbid obesity despite receiving replacement doses of glucocorticoids. Urine analysis of cortisol and cortisone metabolites show that 11-OH/11-oxo ratios are significantly higher in patients with hypothalamic obesity, indicating enhanced 11beta-HSD1 activity. This correlates with the visceral-to-subcutaneous fat ratio. The consequence of increased 11beta-HSD1 activity and a shift of the steroid inter-conversion towards cortisol may contribute to the effects of the latter in adipose tissue. The message from the hypothalamus to adipocyte 11beta-HSD-1 involves hormones, the sympathetic nervous system and cytokines. CRH and ACTH downregulate 11beta-HSD-1 activity and induce lipolysis. Tumor necrosis factor-alpha and interleukin-1beta upregulate 11beta-HSD-1 expression and activity, while enhancing lipolysis. The sympathetic nervous system exerts its effects through beta-adrenergic upregulation and alpha-adrenergic downregulation of 11beta-HSD-1 activity. Inhibition of 11beta-HSD-1 suppresses preadipocyte differentiation into mature adipocytes, and may provide a therapeutic tool.lld:pubmed
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pubmed-article:15241725pubmed:articleTitleHypothalamic regulation of adiposity: the role of 11beta-hydroxysteroid dehydrogenase type 1.lld:pubmed
pubmed-article:15241725pubmed:affiliationDivision of Endocrinology, Meyer Children's Hospital, PO Box 9602, Rambam Medical Center, Haifa 31096, Israel. z_hochberg@rambam.health.gov.illld:pubmed
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