Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-9-7
pubmed:abstractText
Leptin receptors are distributed throughout the body and leptin has been shown to have various effects. As we have recently demonstrated a positive correlation between serum leptin levels and TSH in euthyroid subjects, we investigated the effect of leptin on the thyroids. It was observed that serum leptin levels were negatively correlated with free thyroxine/TSH ratios in the serum of euthyroid female subjects. This suggests that leptin may modulate TSH effects. RT-PCR for leptin receptor expression revealed that FRTL-5 cells possess the gene transcript to the long cytoplasmic form of the receptor. Leptin actually appeared to induce an increase in c-fos mRNA expression. However, it inhibited iodide uptake typically induced by both TSH and dibutyryl cAMP, while leptin did not inhibit TSH-induced cAMP production or TSH-stimulated DNA synthesis in 4H medium (in the absence of insulin and TSH). Leptin also was observed to inhibit TSH- and dibutyryl cAMP-induced Na+/I- symporter and thyroglobulin mRNA expression. Lastly, leptin was seen to inhibit TSH-stimulated thymidine incorporation in 5H medium. Taken together, these results suggest that leptin suppresses TSH-induced thyroid function. Therefore, we hypothesized that leptin may be one of the regulators of thyroid function in obese patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Bucladesine, http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP, http://linkedlifedata.com/resource/pubmed/chemical/DNA, http://linkedlifedata.com/resource/pubmed/chemical/Iodides, http://linkedlifedata.com/resource/pubmed/chemical/Leptin, 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/Recombinant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Symporters, http://linkedlifedata.com/resource/pubmed/chemical/Thyroglobulin, http://linkedlifedata.com/resource/pubmed/chemical/Thyroid Hormones, http://linkedlifedata.com/resource/pubmed/chemical/Thyrotropin, http://linkedlifedata.com/resource/pubmed/chemical/Thyroxine, http://linkedlifedata.com/resource/pubmed/chemical/leptin receptor, human, http://linkedlifedata.com/resource/pubmed/chemical/sodium-iodide symporter
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0918-8959
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
415-23
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15351798-Animals, pubmed-meshheading:15351798-Bucladesine, pubmed-meshheading:15351798-Cell Line, pubmed-meshheading:15351798-Cyclic AMP, pubmed-meshheading:15351798-DNA, pubmed-meshheading:15351798-Female, pubmed-meshheading:15351798-Gene Expression, pubmed-meshheading:15351798-Genes, fos, pubmed-meshheading:15351798-Humans, pubmed-meshheading:15351798-Iodides, pubmed-meshheading:15351798-Leptin, pubmed-meshheading:15351798-RNA, Messenger, pubmed-meshheading:15351798-Rats, pubmed-meshheading:15351798-Receptors, Cell Surface, pubmed-meshheading:15351798-Receptors, Leptin, pubmed-meshheading:15351798-Recombinant Proteins, pubmed-meshheading:15351798-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15351798-Symporters, pubmed-meshheading:15351798-Thyroglobulin, pubmed-meshheading:15351798-Thyroid Gland, pubmed-meshheading:15351798-Thyroid Hormones, pubmed-meshheading:15351798-Thyrotropin, pubmed-meshheading:15351798-Thyroxine
pubmed:year
2004
pubmed:articleTitle
Leptin regulation of the thyroids: negative regulation on thyroid hormone levels in euthyroid subjects and inhibitory effects on iodide uptake and Na+/I- symporter mRNA expression in rat FRTL-5 cells.
pubmed:affiliation
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't