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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
22
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pubmed:dateCreated |
2006-5-31
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pubmed:abstractText |
To elucidate whether the role of leptin in regulating neuroendocrine and immune function during short-term starvation in healthy humans is permissive, i.e., occurs only when circulating leptin levels are below a critical threshold level, we studied seven normal-weight women during a normoleptinemic-fed state and two states of relative hypoleptinemia induced by 72-h fasting during which we administered either placebo or recombinant methionyl human leptin (r-metHuLeptin) in replacement doses. Fasting for 72 h decreased leptin levels by approximately = 80% from a midphysiologic (14.7 +/- 2.6 ng/ml) to a low-physiologic (2.8 +/- 0.3 ng/ml) level. Administration of r-metHuLeptin during fasting fully restored leptin to physiologic levels (28.8 +/- 2.0 ng/ml) and reversed the fasting-associated decrease in overnight luteinizing hormone pulse frequency but had no effect on fasting-induced changes in thyroid-stimulating hormone pulsatility, thyroid and IGF-1 hormone levels, hypothalamic-pituitary-adrenal and renin-aldosterone activity. FSH and sex steroid levels were not altered. Short-term reduction of leptin levels decreased the number of circulating cells of the adaptive immune response, but r-metHuLeptin did not have major effects on their number or in vitro function. Thus, changes of leptin levels within the physiologic range have no major physiologic effects in leptin-replete humans. Studies involving more severe and/or chronic leptin deficiency are needed to precisely define the lower limit of normal leptin levels for each of leptin's physiologic targets.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-10084566,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-10523015,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-10525043,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-10644535,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-11334904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-11443202,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-11923112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-11994393,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-12121659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-12393845,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-12519869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-12658369,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-12727933,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15070752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15070944,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15342807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15531489,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15592472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15613409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15690321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-15699332,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-6965559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-7714088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-7984236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-8157720,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-8589726,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-8717038,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16714386-9732873
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
30
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pubmed:volume |
103
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
8481-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16714386-Adaptation, Physiological,
pubmed-meshheading:16714386-Adipose Tissue,
pubmed-meshheading:16714386-Adult,
pubmed-meshheading:16714386-Body Fat Distribution,
pubmed-meshheading:16714386-Body Weight,
pubmed-meshheading:16714386-Cells, Cultured,
pubmed-meshheading:16714386-Fasting,
pubmed-meshheading:16714386-Female,
pubmed-meshheading:16714386-Hormones,
pubmed-meshheading:16714386-Humans,
pubmed-meshheading:16714386-Immunity,
pubmed-meshheading:16714386-Immunity, Innate,
pubmed-meshheading:16714386-Insulin-Like Growth Factor I,
pubmed-meshheading:16714386-Leptin,
pubmed-meshheading:16714386-Leukocyte Count,
pubmed-meshheading:16714386-Neurosecretory Systems,
pubmed-meshheading:16714386-T-Lymphocytes,
pubmed-meshheading:16714386-Time Factors
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pubmed:year |
2006
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pubmed:articleTitle |
Differential regulation of metabolic, neuroendocrine, and immune function by leptin in humans.
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pubmed:affiliation |
Division of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
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pubmed:publicationType |
Journal Article,
Controlled Clinical Trial,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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