Hormonal regulation of the novel adipocytokine visfatin in 3T3-L1 adipocytes

J Endocrinol. 2005 Jun;185(3):R1-8. doi: 10.1677/joe.1.06211.

Abstract

Recently, visfatin was characterized as a novel adipo-cytokine that is upregulated in obesity and exerts insulin-mimetic effects in various tissues. To clarify expression and regulation of this adipocytokine, visfatin mRNA was measured by quantitative real-time reverse transcription-polymerase chain reaction in 3T3-L1 adipocytes during adipogenesis and after treatment with various hormones known to alter insulin sensitivity. Visfatin expression was about 6-fold higher in 3T3-L1 adipocytes in vitro as compared with epididymal fat in vivo and increased during adipogenic conversion more than 3-fold. Interestingly, 100 nM dexamethasone significantly increased visfatin mRNA by almost 1.5-fold. In contrast, 500 ng/ml growth hormone (GH), 10 ng/ml tumor necrosis factor (TNF) alpha, and 10 microM isoproterenol downregulated visfatin expression by 45%, 36%, and 43% respectively. Insulin did not influence synthesis of this adipocytokine. The effects of dexamethasone, GH, TNFalpha and isoproterenol were time- and dose-dependent. Furthermore, activation of G(s)-protein-coupled pathways by forskolin and cholera toxin was sufficient to significantly downregulate visfatin mRNA. Taken together, our results show a differential regulation of visfatin mRNA by insulin resistance-inducing hormones, supporting the view that this adipo-cytokine might be an interesting novel candidate linking core components of the metabolic syndrome such as obesity and insulin resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Adrenergic beta-Agonists / pharmacology
  • Animals
  • Cell Culture Techniques
  • Cell Differentiation
  • Cholera Toxin / pharmacology
  • Colforsin / pharmacology
  • Cyclic AMP / metabolism
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Depression, Chemical
  • Dexamethasone / pharmacology*
  • Dose-Response Relationship, Drug
  • GTP-Binding Protein alpha Subunits, Gs / metabolism
  • Gene Expression Regulation / drug effects*
  • Glucocorticoids / pharmacology*
  • Growth Hormone / pharmacology
  • Isoproterenol / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Nicotinamide Phosphoribosyltransferase
  • RNA, Messenger / analysis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Adrenergic beta-Agonists
  • Cytokines
  • Glucocorticoids
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Colforsin
  • Dexamethasone
  • Growth Hormone
  • Cholera Toxin
  • Cyclic AMP
  • Nicotinamide Phosphoribosyltransferase
  • nicotinamide phosphoribosyltransferase, mouse
  • GTP-Binding Protein alpha Subunits, Gs
  • Isoproterenol