Inhibition by insulin of resistin gene expression in 3T3-L1 adipocytes

• Published in: FEBS letters 2001-10, Vol.507 (1), p.105-108
• Main Authors: Haugen, Fred, Jørgensen, Aud, Drevon, Christian A, Trayhurn, Paul
• Format: Article
• Language: English
• Subjects: 3T3 Cells; Adipocyte; Adipocytes - cytology; Adipocytes - drug effects; Adipocytes - metabolism; Animals; Base Sequence; Cell Differentiation; Dexamethasone; Diabetes; DNA, Complementary - genetics; Gene Expression Regulation - drug effects; Hormones, Ectopic - genetics; Humans; Insulin; Insulin - pharmacology; Insulin Resistance - physiology; Intercellular Signaling Peptides and Proteins; Male; Mice; Mice, Inbred C57BL; Mice, Inbred CBA; Nerve Growth Factor; Oligodeoxyribonucleotides, Antisense - genetics; Proteins; Resistin; RNA, Messenger - genetics; RNA, Messenger - metabolism; Tissue Distribution; β-Adrenoceptor agonist
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(01)02968-4

Expression of the gene encoding resistin, a low molecular weight protein secreted from adipose tissue postulated to link obesity and type II diabetes, was examined in 3T3-L1 adipocytes. Resistin mRNA was detected in 3T3-L1 cells by day 3 following induction of differentiation into adipocytes; by day 4 the level of resistin mRNA peaked and remained high. The PPARγ activators, rosiglitazone or darglitazone, reduced the level of resistin mRNA. Dexamethasone upregulated resistin mRNA level, but no effect was observed with the β 3-adrenoceptor agonist, BRL 37344. A substantial reduction in resistin mRNA level was observed with insulin, which induced decreases at physiological concentrations. Insulin may be a major inhibitor of resistin production, and this does not support a role for resistin in insulin resistance.