Effect of tri-iodothyronine on leptin release and leptin mRNA accumulation in rat adipose tissue

Leptin, the product of the obese gene, is produced by white adipocytes. The release of leptin, as well as leptin mRNA content, was enhanced in adipocytes isolated from hypothyroid rats. The administration of tri-iodothyronine (T3) 8 h before death inhibited leptin release by adipocytes incubated for...

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Bibliographic Details
Published in:Biochemical journal 1998-06, Vol.332 (2), p.361-366
Main Authors: Fain, J.N, Bahouth, S.W
Format: Article
Language:English
Subjects:
adipocytes
Adipocytes - drug effects
Adrenergic beta-Agonists - pharmacology
Animals
Dexamethasone - pharmacology
Dioxoles - pharmacology
Glyceraldehyde-3-Phosphate Dehydrogenases - metabolism
Hypothyroidism - physiopathology
Insulin - pharmacology
Leptin
Lipolysis - drug effects
Male
messenger RNA
obesity
Proteins - metabolism
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
RNA, Ribosomal, 18S - metabolism
Triiodothyronine - pharmacology
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Summary:Leptin, the product of the obese gene, is produced by white adipocytes. The release of leptin, as well as leptin mRNA content, was enhanced in adipocytes isolated from hypothyroid rats. The administration of tri-iodothyronine (T3) 8 h before death inhibited leptin release by adipocytes incubated for 6 or 24 h. Direct addition of T3 to pieces of adipose tissue enhanced the loss of leptin mRNA seen over 24 h in the presence of dexamethasone plus the beta3-adrenergic agonist Cl 316,243. In contrast, if pieces of adipose tissue were incubated with dexamethasone plus insulin, enhanced the T3 accumulation of leptin mRNA. These results indicate that T3 enhances net adipocyte leptin mRNA accumulation in a condition that approximates the fed state (presence of insulin) but inhibits leptin mRNA accumulation in a condition that approximates the fasted state (absence of insulin).
ISSN:0264-6021
1470-8728
DOI:10.1042/bj3320361