Summary
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), non-esterified 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 (Δ IRI area 0-5 min) and late (Δ 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.
Key-Words:
Acetylsalicylic Acid
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Insulin
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C-Peptide
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Pancreatic Glucagon
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Growth Hormone
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Non-Esterified Fatty Acids
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Glucose Infusion
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Glucose Tolerance
