Abstract

To determine the effects of islet cell antibodies on beta-cell function during the first 3 yr after diagnosis in type II diabetic patients. beta-cell function in type II diabetic patients with (n = 11, 50 +/- 5 yr of age) and without (n = 10, 52 +/- 4 yr of age) ICA was followed prospectively and compared with beta-cell function in type I adult diabetic patients (n = 17, 37 +/- 5 yr of age) and in healthy control subjects (n = 34, age 45 +/- 3 yr). beta-cell function was evaluated as fasting C-peptide, 1 + 3 min C-peptide after intravenous glucose, and delta C-peptide after glucagon. Fasting C-peptide was equal in type II diabetic patients with ICA (0.30 +/- 0.03 nM) and type I diabetic patients (0.24 +/- 0.03 nM) at diagnosis, and decreased (P < 0.05) during 3 yr in these groups but not in type II diabetic patients without ICA. At diagnosis, type II diabetic patients with ICA showed a 1 + 3 min C-peptide (0.92 +/- 0.17 nM) lower (P < 0.001) than control subjects but higher (P < 0.05) than type I diabetic patients (0.53 +/- 0.11 nM). After 1 yr, 1 + 3 min C-peptide in type II diabetic patients with ICA had decreased (P < 0.05) to 0.18 +/- 0.11 nM and was equal to type I diabetic patients (0.38 +/- 0.10 nM). delta C-peptide after glucagon was equally impaired in type II diabetic patients with ICA (0.38 +/- 0.06 nM) and type I diabetic patients (0.35 +/- 0.11 nM) at diagnosis. After 3 yr, type II diabetic patients with ICA had fasting C-peptide of 0.09 +/- 0.04 nM, 1 + 3 min C-peptide of 0.18 +/- 0.10 nM, and delta C-peptide after glucagon of 0.20 +/- 0.09 nM, values equal to type I diabetic patients but lower (P < 0.01) than in type II diabetic patients without ICA, whose values remained unchanged; fasting C-peptide of 0.97 +/- 0.17 nM, 1 + 3 min C-peptide of 2.31 +/- 0.50 nM, and delta C-peptide after glucagon of 1.76 +/- 0.28 nM. In patients considered type II diabetic with ICA, beta-cell function progressively decreased after diagnosis, and after 3 yr was similar to type I diabetic patients, whereas beta-cell function in type II diabetic patients without ICA was unchanged.

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