Melatonin effects on metabolism independent of gonad function
We previously demonstrated that daily melatonin administration to middle-aged rats, restoring nocturnal plasma melatonin to young adult levels, decreased body weight and suppressed visceral fat and plasma leptin. In some species, metabolic and some neuronal responses to melatonin are mediated or dep...
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Published in: | Endocrine Vol. 21; no. 2; pp. 169 - 173 |
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Main Authors: | , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
01-07-2003
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Subjects: | |
Online Access: | Get full text |
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Summary: | We previously demonstrated that daily melatonin administration to middle-aged rats, restoring nocturnal plasma melatonin to young adult levels, decreased body weight and suppressed visceral fat and plasma leptin. In some species, metabolic and some neuronal responses to melatonin are mediated or dependent at least in part on gonadal steroid levels. Thus, melatonin-induced changes in gonadal steroid secretion may have mediated the aging-dependent melatonin-induced metabolic responses in our previous studies. To address this issue, melatonin (0.4 micro g/mL) or vehicle (0.01% ethanol) was administered for 10 wk in the drinking water of both castrate and sham-operated Sprague-Dawley male rats, starting 1 mo after surgery at 9 mo of age. Melatonin treatment decreased (p < 0.05) body weight in sham-operated rats by 7 +/- 2% relative to control (n = 7/treatment), comparable to our previous results; melatonin likewise decreased (p < 0.05) body weight in castrate rats by 6 +/- 2% relative to control (n = 7/treatment). Melatonin treatment also decreased both intraabdominal fat and plasma leptin levels in both intact and castrate rats, with no significant differences of percentage suppression in the intact versus castrate rats. These results demonstrate that suppression of body weight, visceral adiposity, and plasma leptin levels by daily melatonin administration to middle-aged rats was independent of gonadal function. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1355-008X |
DOI: | 10.1385/ENDO:21:2:169 |