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Transcapillary insulin transfer in human skeletal muscle
Article first published online: 13 FEB 2003
DOI: 10.1046/j.1365-2362.2003.01106.x
Additional Information
How to Cite
Herkner, H., Klein, N., Joukhadar, C., Lackner, E., Langenberger, H., Frossard, M., Bieglmayer, C., Wagner, O., Roden, M. and Müller, M. (2003), Transcapillary insulin transfer in human skeletal muscle. European Journal of Clinical Investigation, 33: 141–146. doi: 10.1046/j.1365-2362.2003.01106.x
Publication History
- Issue published online: 13 FEB 2003
- Article first published online: 13 FEB 2003
- Received 29 November 2001; accepted 9 September 2002
- Abstract
- Article
- References
- Cited By
Keywords:
- Glucose intolerance;
- interstitium;
- metabolic syndrome;
- transendothelial
Abstract
Background Transcapillary insulin transfer is considered a rate-limiting step in insulin action at supraphysiological insulin concentrations. However, it remains unclear whether this concept also applies for physiological conditions.
Materials and methods In the present study we set out to characterize transcapillary insulin transfer by measuring insulin concentrations in plasma and interstitial space fluid of skeletal muscle during an oral glucose tolerance test and euglycaemic hyperinsulinaemic clamp conditions, respectively. For this purpose we employed in vivo microdialysis of skeletal muscle in conjunction with an ultrasensitive insulin assay in eight healthy lean male volunteers (aged 25 ± 1 years).
Results Insulin concentrations at baseline were 48 ± 8 pmol L−1 in plasma and 19 ± 4 pmol L−1 in the interstitium (P = 0·002). The mean interstitium to plasma ratio at baseline was 0·48 ± 0·09 pmol L−1. During the oral glucose tolerance test the interstitium to plasma ratio remained unchanged (0·43 ± 0·12, P = NS vs. baseline), but was significantly reduced during euglycaemic hyperinsulinaemic clamp conditions at steady-state hyperinsulinaemia (0·12 ± 0·01, P = 0·01 vs. baseline).
Conclusion In summary there is a substantial transcapillary insulin gradient in healthy human skeletal muscle under baseline and glucose-stimulated conditions. Our findings support the hypothesis of a saturable transcapillary insulin transport representing a partly rate-limiting step for insulin action.