Source:http://linkedlifedata.com/resource/pubmed/id/14657608
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2003-12-5
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pubmed:abstractText |
Neonatal L-monosodium glutamate (MSG) administration in rats induces several neuroendocrine and metabolic disruptions. Leptin, the adipocyte product, modulates several neuroendocrine systems including the hypothalamic-pituitary-gonadal (HPG) axis in mammals. The aim of the present study was to determine whether MSG-induced chronic hyperleptinemia could play any relevant role in the hypogonadism developed by male rats when examined in adulthood. We found that 120-day-old MSG male rats displayed significant hyperleptinemia, hypogonadism, and undisturbed basic testis structure and spermatogenesis. In vitro studies in purified Leydig cells from normal (CTR) and MSG-damaged rats revealed that basal and human chorionic gonadotropin (hCG)-stimulated 17-hydroxy-progesterone (17-HO-P(4)), Delta(4)-androstenedione (Delta(4)A) and testosterone (T) secretions were significantly lower in MSG than in CTR cells. Exposure to murine leptin (Mleptin, 10(-8)M) significantly inhibited hCG-elicited T secretion by CTR cells after 180 min incubation. While Mleptin significantly inhibited hCG-stimulated Delta(4)A output and the Delta(4)A:17-OH-P(4) ratio of secretion, conversely, it failed to modify the ratio T:Delta(4)A release by CTR Leydig cells. Interestingly, the effects of Mleptin found on CTR Leydig cells were absent in MSG Leydig cells. Finally, endogenous hyperleptinemia was associated with a significant decrease in Leydig cell expression of Ob-Rb mRNA in MSG rats. In summary, this study demonstrates that: (1) Mleptin inhibited testicular steroidogenesis in CTR rats; (2) MSG-treated rats showed lower in vitro 17-OH-P(4), Delta(4)A and T production under basal and post-hCG stimulation conditions; (3) purified Leydig cells from MSG-treated rats displayed resistance to the inhibitory action of Mleptin on T release, and (4) endogenous leptin exerts a modulatory effect on Leydig cell Ob-Rb mRNA expression. The inhibitory effect of leptin on testicular function is thus abrogated in MSG-damaged rats. The testicular leptin-resistance developed by MSG rats seems to be due to early chronic exposure of Leydig cells to high leptin circulating levels, which in turn down-regulate testicular Ob-Rb expression. It remains to be determined whether the testicular dysfunction of MSG rats can be reversed after correction of hyperleptinemia or whether it is an irreversible effect of the hypothalamic lesion.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Androstenols,
http://linkedlifedata.com/resource/pubmed/chemical/Follicle Stimulating Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Luteinizing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Testosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Thyroxine,
http://linkedlifedata.com/resource/pubmed/chemical/androsta-5,16-dien-3 beta-ol,
http://linkedlifedata.com/resource/pubmed/chemical/leptin receptor, human,
http://linkedlifedata.com/resource/pubmed/chemical/leptin receptor, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0028-3835
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2003 S. Karger AG, Basel
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pubmed:issnType |
Print
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
270-9
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:14657608-Analysis of Variance,
pubmed-meshheading:14657608-Androstenols,
pubmed-meshheading:14657608-Animals,
pubmed-meshheading:14657608-Animals, Newborn,
pubmed-meshheading:14657608-Blotting, Northern,
pubmed-meshheading:14657608-Body Weight,
pubmed-meshheading:14657608-Disease Models, Animal,
pubmed-meshheading:14657608-Dose-Response Relationship, Drug,
pubmed-meshheading:14657608-Female,
pubmed-meshheading:14657608-Follicle Stimulating Hormone,
pubmed-meshheading:14657608-Hypogonadism,
pubmed-meshheading:14657608-Leptin,
pubmed-meshheading:14657608-Leydig Cells,
pubmed-meshheading:14657608-Luteinizing Hormone,
pubmed-meshheading:14657608-Male,
pubmed-meshheading:14657608-Mice,
pubmed-meshheading:14657608-Organ Size,
pubmed-meshheading:14657608-RNA, Messenger,
pubmed-meshheading:14657608-Radioimmunoassay,
pubmed-meshheading:14657608-Rats,
pubmed-meshheading:14657608-Rats, Sprague-Dawley,
pubmed-meshheading:14657608-Receptors, Cell Surface,
pubmed-meshheading:14657608-Receptors, Leptin,
pubmed-meshheading:14657608-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:14657608-Sodium Glutamate,
pubmed-meshheading:14657608-Testis,
pubmed-meshheading:14657608-Testosterone,
pubmed-meshheading:14657608-Thyroxine
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pubmed:year |
2003
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pubmed:articleTitle |
Modulatory effects of leptin on leydig cell function of normal and hyperleptinemic rats.
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pubmed:affiliation |
Instituto Multidisciplinario de Biología Celular, La Plata, Argentina.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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