Diabetologia

, Volume 41, Issue 5, pp 560–568

Various phosphodiesterase subtypes mediate the in vivo antilipolytic effect of insulin on adipose tissue and skeletal muscle in man

Authors

  • S. Enoksson
    • Department of Vascular Surgery, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden
  • E. Degerman
    • Department for Cell and Molecular Biology, Section for Molecular Signalling, Lund University, Lund, Sweden
  • E. Hagström-Toft
    • Department for Cell and Molecular Biology, Section for Molecular Signalling, Lund University, Lund, Sweden
  • V. Large
    • Department of Medicine and Research Center, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden
  • P. Arner
    • Department of Medicine and Research Center, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden
Originals

DOI: 10.1007/s001250050947

Cite this article as:
Enoksson, S., Degerman, E., Hagström-Toft, E. et al. Diabetologia (1998) 41: 560. doi:10.1007/s001250050947

Summary

The antilipolytic effect of insulin on human abdominal subcutaneous adipose tissue and skeletal muscle during local inhibition of cAMP-phosphodiesterases (PDEs) was investigated in vivo, by combining microdialysis with a euglycaemic, hyperinsulinaemic clamp. During hyperinsulinaemia, the glycerol concentration decreased by 40 % in fat and by 33 % in muscle. Addition of the selective PDE3-inhibitor amrinone abolished the insulin-induced decrease in adipose glycerol concentration, but did not influence the glycerol concentration in skeletal muscle. Nor did the PDE4-selective inhibitor rolipram or the PDE5-selective inhibitor dipyridamole influence the insulin-induced decrease in muscle tissue glycerol. However, the non-selective PDE-inhibitor theophylline counteracted the antilipolytic action of insulin at both sites. The specific activity of PDEs was also determined in both tissues. PDE3-activity was 36.8 ± 6.4 pmol × min–1× mg–1 in adipose tissue and 3.9 ± 0.5 pmol × min–1× mg–1 in muscle. PDE4-activity in skeletal muscle was high, i. e., 60.7 ± 10.2 pmol × min–1× mg–1 but 8.5 pmol × min–1× mg–1 or less in adipose tissue. In conclusion, insulin inhibits lipolysis in adipose tissue and skeletal muscle by activation of different PDEs, suggesting a unique metabolic role of muscle lipolysis. [Diabetologia (1998) 41: 560–568]

Keywords Microdialysisglycerolinterstitial flowphosphodiesterase inhibitors.
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Copyright information

© Springer-Verlag Berlin Heidelberg 1998