Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-7-22
pubmed:abstractText
The physiological consequences and mechanism(s) for thyroid hormone-induced alterations in serum leptin are not known. To address this, leptin expression in rats was evaluated in relationship to food intake, fat mass, and body temperature in rats with pharmacologically altered thyroid status. Total body weight, food intake, and temperature were decreased in hypothyroid rats. Fat weight was decreased in both chronically hypothyroid and hyperthyroid rats (n = 6/group). Serum leptin was linearly correlated with fat weight, epididymal and retroperitoneal fat leptin mRNA concentration, but not total body weight. Serum leptin was decreased in the chronically hyperthyroid rats. When fat weight was used as a covariant, serum leptin was not different between the three groups. Epididymal fat leptin mRNA was higher in euthyroid (n = 7) than in hypothyroid and hyperthyroid rats. Retroperitoneal fat leptin mRNA was not affected by thyroid status. A positive linear relationship between food intake and free triiodothyronine (FT3) index was observed, but not between food intake and serum leptin alone. In a time course study, serum leptin, epididymal fat leptin mRNA content, and fat weight did not change within 24 hours of high-dose triiodothyronine (T3) (n = 6/group), but both temperature and epididymal fat S14 mRNA content rapidly increased. These findings demonstrate that thyroid state influences circulating leptin levels, but primarily does so indirectly through the regulation of fat mass. Leptin does not influence core body temperature across thyroidal state. Finally, thyroid state is more important to regulate food intake, through an as yet undefined mechanism, than are thyroid state-associated changes in serum leptin.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1050-7256
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
503-12
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10365683-Adipose Tissue, pubmed-meshheading:10365683-Animals, pubmed-meshheading:10365683-Body Temperature, pubmed-meshheading:10365683-Body Weight, pubmed-meshheading:10365683-Energy Intake, pubmed-meshheading:10365683-Humans, pubmed-meshheading:10365683-Hyperthyroidism, pubmed-meshheading:10365683-Hypothyroidism, pubmed-meshheading:10365683-Leptin, pubmed-meshheading:10365683-Male, pubmed-meshheading:10365683-Organ Size, pubmed-meshheading:10365683-Proteins, pubmed-meshheading:10365683-RNA, Messenger, pubmed-meshheading:10365683-Rats, pubmed-meshheading:10365683-Rats, Sprague-Dawley, pubmed-meshheading:10365683-Regression Analysis, pubmed-meshheading:10365683-Thyroid Gland, pubmed-meshheading:10365683-Transcription, Genetic, pubmed-meshheading:10365683-Triiodothyronine
pubmed:year
1999
pubmed:articleTitle
The effect of thyroid hormone on size of fat depots accounts for most of the changes in leptin mRNA and serum levels in the rat.
pubmed:affiliation
Department of Medicine, University of Pittsburgh School of Medicine, Pennsylvania 15261, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't