Failure of indomethacin to affect arginine-induced C-peptide and glucagon release in insulin-treated diabetics. Major role of residual B cell function in conditioning the magnitude of the blood glucose rise after intravenous arginine.

Fourteen insulin-treated diabetics were submitted to an arginine infusion test performed with either 11.7 or 5.85 mg kg-1 min-1 arginine monohydrochloride infused during 40 min with or without previous oral administration of a low (75 + 50 mg) or a high (75 mg + 3 mg/kg) dose of indomethacin. Blood glucose, plasma non-esterified fatty acids, insulin, C-peptide and glucagon were determined at regular intervals before, during and after the arginine infusion. These parameters were totally unaffected by the two doses of indomethacin both in the basal state and during the arginine infusions at the two loads tested. Eight subjects had a basal C-peptide level above 0.07 pmol/ml and a mean (+/- SEM) maximal rise of 0.21 +/- 0.04 pmol/ml during the arginine infusion, whereas the remaining six patients had virtually zero values throughout the tests. The arginine-induced plasma glucagon rise was similar for the two rates of arginine infusion; the sum of the increments in plasma glucagon averaged 877 +/- 120 and 647 +/- 92 pg/ml (p greater than 0.1) for the high and low rates of arginine infusion, respectively. The magnitude of the blood glucose rise appeared independent of the amount of arginine infused. Confirming previous reports, we found that the blood glucose rise after arginine was three to four times higher in subjects without C-peptide than in subjects with C-peptide. The mean glucagon response did not differ significantly between subjects with or without C-peptide. Thus, residual B cell function determines the magnitude of the blood glucose rise but not the glucagon response after intravenous arginine.