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

Author:

FAIN John N.1,BAHOUTH Suleiman W.2

Affiliation:

1. Department of Biochemistry, College of Medicine, University of Tennessee, Memphis, TN 38163, U.S.A.

2. Department of Pharmacology, College of Medicine, University of Tennessee, Memphis, TN 38163, U.S.A.

Abstract

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 β3-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).

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

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