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

  • S. Enoksson
  • E. Degerman
  • E. Hagström-Toft
  • V. Large
  • P. Arner
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

Authors and Affiliations

  • S. Enoksson
    • 1
  • E. Degerman
    • 2
  • E. Hagström-Toft
    • 2
  • V. Large
    • 3
  • P. Arner
    • 3
  1. 1.Department of Vascular Surgery, Huddinge University Hospital, Karolinska Institute, Huddinge, SwedenSE
  2. 2.Department for Cell and Molecular Biology, Section for Molecular Signalling, Lund University, Lund, SwedenSE
  3. 3.Department of Medicine and Research Center, Huddinge University Hospital, Karolinska Institute, Huddinge, SwedenSE