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Peripheral Insulin Parallels Changes in Insulin Secretion More Closely Than C-Peptide After Bolus Intravenous Glucose Administration^*

E. TIMOTHY SHAPIRO, HARTMUT TILLIL, ARTHUR H. RUBENSTEIN and KENNETH S. POLONSKY

Department of Medicine, University of Chicago, Pritzker School of Medicine Chicago, Illinois 60637

Address all correspondence and requests for reprints to: Kenneth S. Polonsky, M.D., Department of Medicine, Box 435, University of Chicago, 5841 South Maryland Avenue, Chicago, Illinois 60637.

The changes in peripheral serum insulin and plasma C-peptide levels and in the insulin secretory rate in response to iv glucose (0.5 g/kg BW) administration were studied in seven normal subjects. Insulin secretory rates were calculated according to a two-compartment model of distribution for Cpeptide, using individual C-peptide kinetics calculated from iv bolus injections of biosynthetic human C-peptide.

The mean plasma glucose level increased from a fasting level of 5.1 ± 0.1 (±SE) to a peak of 24.0 ± 1.0 mmol/L at 3 min and reached basal levels 101 ± 6 min after glucose administration. The mean serum insulin value increased from 50 ± 12 to a peak of 405 ± 58 pmol/L at 3 min and then declined to fasting levels 139 ± 14 min after the stimulus. In contrast, the mean plasma C-peptide level increased from 390 ± 50 to a peak of 1460 ± 210 pmol/L at 3 min and only began declining 45 min after glucose administration, reaching fasting levels 191 ± 15 min after the stimulus. The mean insulin secretory rate increased from 69.8 ± 19.9 to a peak of 1412.7 ± 159.1 pmol/min at 3 min (15.3 ± 2.5-fold elevation over baseline) and reached basal levels 135 ± 12 min after the stimulus. The clearance of endogenous insulin during the basal period (2.505 ± 0.365 L/min) and that during the 4 h after the stimulus (2.319 ± 0.230 L/min) were similar.

In conclusion, after bolus iv glucose administration: 1) the insulin secretory rate is more closely represented by changes in peripheral serum insulin than in plasma C-peptide levels; and 2) no change in endogenous insulin clearance occurs.

^* This work was supported in part by Grant DK-31842 from the NIH, the Diabetes Research and Training Center (DK-20595), and the Clinical Research Center at the University of Chicago (RR-00055).

Supported by the Deutsche Forschungsgemeinschaft (Training Grant Ti 154/1-1) and the Deutsche Diabetes-Gesellschaft (Junior Science Award).

Recipient of a Research Career Development Award from the NIH (DK-01234).

Received January 27, 1988.

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