Discrepant effect of the prostaglandin synthesis inhibitor acetylsalicylic acid on insulin and C-peptide response to glucose in man.

The prostaglandin synthesis inhibitor acetylsalicylic acid (ASA) increases acute insulin response to glucose and improves glucose tolerance in man. In an effort to provide further information on the mechanism whereby ASA improves glucose tolerance, we studied the effect of ASA on C-peptide, insulin, pancreatic glucagon (IRG), growth hormone (HGH), nonesterified fatty acids (NEFA) and glycerol responses to glucose in 11 non-obese subjects with impaired glucose tolerance. The glucose tolerance was evaluated by means of a 2 h-glucose infusion test. A daily treatment with 3.0 g ASA over 3 days caused a significant increase of acute (delta IRI area 0-5 min) and late (delta IRI area 30-120 min) insulin response and an improvement of glucose tolerance. By contrast, C-peptide response was in the same range prior to and after ASA treatment. Thus, the C-peptide/insulin ratio was decreased by about 50% due to ASA treatment. IRG, HGH, NEFA and glycerol responses to glucose were not altered by ASA treatment. In summary, the discrepant effect of ASA on C-peptide and insulin responses suggest that changes of insulin metabolism may be involved in the mechanism of ASA induced increase in peripheral insulin levels. The improvement of glucose tolerance after ASA application seems to be related to the biologic effect of higher circulating insulin levels but not to alteration of insulin antagonists, such as IRG, HGH and NEFA.