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Background: The purpose of this prospective open-label trial was (1) to assess the Influence of oral antidiabetic drugs (OAD) on the glycemic index (GI), glucose response curves (GRCs), daily mean plasma glucose (MPG) and (2) to compare the GI of foods in persons with OAD-treated type 2 diabetes mellitus (T2DM) with the respective GI in healthy persons (HP). Methods: Tested foods containing 50 g of carbohydrates were eaten for breakfast and dinner after 10 and 4 h of fasting, respectively. Glycemic index, GRC, and MPG were obtained using the CGMS® System Gold™ (CGMS). In T2DM patients [n = 16; age (mean ± standard error) 56.0 ± 2.25 years], foods were tested four times: tests 1, 2, and 3 were performed within one week in which placebo was introduced on day 2, and test 4 was carried out five weeks after reintroduction of OAD. Glycemic indexes, GRC, and MPG from tests 1, 2, 3, and 4 were compared. In a control group of 20 HP (age 24.4 ± 0.71 years), the mean GIs were calculated as the mean from 20 subject-related GIs. Results: In T2DM patients, subject-related assessment of GIs, GRC, and MPG distinguished persons with and without OAD effect. Nevertheless, the group-related GIs and the MPG on days 2, 8, and 39 showed no significant difference. There was no significant difference between the GIs in OAD-treated T2DM patients (test 4) versus HP (except in apple baby food). Glucose response curves were significantly larger in T2DM patients (test 4) versus HP. Conclusions: Determination of GRC and subject-related GI using the CGMS appears to be a potential means for the evaluation of efficacy of OAD treatment. Further studies are underway.

The age-dependent relationship of fasting immunomeasurable C-peptide to fasting immunomeasurable insulin (IRI) and IRI response to glucose was studied in 113 non-obese healthy subjects with normal glucose tolerance (oGTT according to the new WHO recommendations), ranging in age from 6 to 44 years. Fasting C-peptide concentration increased significantly in adolescents and adults when compared with children. The higher fasting C-peptide concentration in the adult group might be explained by the concomitant higher fasting blood glucose concentration whereas such relationship was lacking in adolescents. In contrast to this we failed to demonstrate such relationship with regard to fasting IRI levels. There was, however, a relationship between advancing age and early (IRI area 0-30 min), late (IRI area 30-120 min) and total (IRI area 0-120 min) insulin response to glucose. There was a significant correlation between fasting C-peptide concentration and estimates of IRI response in children and adolescents, whereas such relationship was lacking in adults. Based on these results, the present study demonstrates an age-related increase of the pancreatic beta-cell function which might be partly explained by the concomitant higher blood glucose concentration.

Since mumps virus seems to be one of the most likely candidates in viral etiology of insulin-dependent diabetes (IDDM) we studied the possible relationship of glucose tolerance (75 g oGTT), beta cell function, diabetes associated HLA antigens, haptoglobin phenotype, islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in 125 subjects with antecedent mumps infection. Impaired glucose tolerance (IGT) was diagnosed in 3.2% (n = 4) but onset of diabetes did not appear within 14 months after mumps infection. There was no relationship between glucose tolerance and complications of antecedent mumps infection (e.g. pancreatitis, meningitis, orchitis). The prevalence rate of ICA was 76%. ICSA were detectable in about 36% of children and 62% of the adults tested (p less than 0.01). There was no relationship between ICA/ICSA and diabetes-associated HLA antigens, haptoglobin phenotype or beta cell function (fasting C-peptide and insulin response to 75 g oGTT). However, adults with circulating ICA were characterized by a significantly lower insulin response to glucose. Fifty two "risk" subjects characterized by IGT, diabetes associated HLA antigen(s), ICA or ICSA either alone or combined were studied again 26 months after mumps infection. No symptomatic diabetes appeared and IGT was diagnosed in one case only. ICA and ICSA persisted in more than 50% of subjects in whom ICA or ICSA were present 14 months after mumps infection. Since the used immunological techniques do not clearly distinguish organ-specific from non-organ-specific antibodies the results must be interpreted with caution. To summarize, the preliminary results do not support a close temporal relationship between mumps infection and the onset of IDDM. The pathogenetic role of mumps virus and ICA/ICSA and their possible relation to a slow progressive beta cell destruction has still to be determined.