The goal of the study was to provide cross-sectional descriptive data on the response of
C-peptide to a vigorous meal stimulus in a population-based sample of nondiabetic adults compared with a population-based sample of adults with
NIDDM. Available information is scanty, especially in subjects greater than 50 yr old.
RESEARCH DESIGN AND METHODS: The group under study included 377 adults without previously known diabetes randomly chosen from the population of the city of Wadena, Minnesota, almost all of northern European background, and 88 adults with known diabetes. PCP was measured 90 min after ingestion of 480 ml liquid meal
Ensure-Plus, which includes 95 g
dextrose, 26
g protein, and 25 g fat.
C-peptide also was measured in a 260-min urine collection after the meal challenge. Novo antibody M1221 was used for
C-peptide assay throughout the study. Participants whose medical record indicated
insulin-dependent diabetes with a history of
acetone production were excluded from analyses.
RESULTS: The distribution of UCP and PCP in this group of subjects appears very broad. Both the highest and lowest values for
C-peptide were observed in individuals with diabetic
glucose tolerance. The mean and median values in the nondiabetic group are higher than in previously published reports. After statistical adjustment for age, sex, BMI, and concomitant plasma
glucose, participants with IGT produced significantly more
C-peptide than the group with NGT (3.48 vs. 2.96 nM PCP, P less than 0.05). Participants with diabetic
glucose tolerance and who were not taking
insulin produced as much or more
C-peptide than either the NGT or IGT groups, depending on the statistical model used for adjusting for plasma
glucose. Diabetic participants who were taking
insulin produced significantly lower amounts of
C-peptide than any of the non-
insulin-taking groups (approximately 30% of the
C-peptide produced by the non-
insulin-taking diabetic participants). A decline in PCP production with increasing years since diagnosis (5.7%/yr) was observed exclusively in the
insulin-taking
NIDDM participants. Effect modification by
glucose tolerance classification was observed on the relationship between plasma
glucose and PCP: PCP increased with increasing plasma
glucose in NGT and IGT groups, but a nonsignificant negative relationship was exhibited in diabetic participants.
CONCLUSIONS: The data suggest that two forms of
NIDDM may exist, crudely distinguished by the clinical decision to use
insulin to
control blood glucose levels. The
insulin-taking diabetic individuals may experience a greater likelihood of pancreatic failure, whereas non-
insulin-taking diabetic individuals probably experience stable pancreatic function over the course of their disease. Longitudinal observation of the Wadena cohort will provide more insight into this possibility.