β-cell function in relation to islet cell antibodies during the first 3 yr after clinical diagnosis of diabetes in type II diabetic patients

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β-cell function in relation to islet cell antibodies during the first 3 yr after clinical diagnosis of diabetes in type II diabetic patients. / Gottsater, A.; Landin-Olsson, M.; Fernlund, P.; Lernmark, A.; Sundkvist, G.

I: Diabetes Care, Vol. 16, Nr. 6, 01.01.1993, s. 902-910.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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T1 - β-cell function in relation to islet cell antibodies during the first 3 yr after clinical diagnosis of diabetes in type II diabetic patients

AU - Gottsater, A.

AU - Landin-Olsson, M.

AU - Fernlund, P.

AU - Lernmark, A.

AU - Sundkvist, G.

PY - 1993/1/1

Y1 - 1993/1/1

N2 - OBJECTIVE - To determine the effects of islet cell antibodies on β-cell function during the first 3 yr after diagnosis in type II diabetic patients. RESEARCH DESIGN AND METHODS - β-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 β-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). β-cell function was evaluated as fasting C- peptide, 1 + 3 min C-peptide after intravenous glucose, and Δ C-peptide after glucagon. RESULTS - 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). Δ 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 Δ 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 Δ C-peptide after glucagon of 1.76 ± 0.28 nM. CONCLUSIONS - In patients considered type II diabetic with ICA, β-cell function progressively decreased after diagnosis, and after 3 yr was similar to type I diabetic patients, whereas β-cell function in type II diabetic patients without ICA was unchanged.

AB - OBJECTIVE - To determine the effects of islet cell antibodies on β-cell function during the first 3 yr after diagnosis in type II diabetic patients. RESEARCH DESIGN AND METHODS - β-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 β-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). β-cell function was evaluated as fasting C- peptide, 1 + 3 min C-peptide after intravenous glucose, and Δ C-peptide after glucagon. RESULTS - 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). Δ 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 Δ 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 Δ C-peptide after glucagon of 1.76 ± 0.28 nM. CONCLUSIONS - In patients considered type II diabetic with ICA, β-cell function progressively decreased after diagnosis, and after 3 yr was similar to type I diabetic patients, whereas β-cell function in type II diabetic patients without ICA was unchanged.

UR - http://www.scopus.com/inward/record.url?scp=0027229335&partnerID=8YFLogxK

U2 - 10.2337/diacare.16.6.902

DO - 10.2337/diacare.16.6.902

M3 - Article

VL - 16

SP - 902

EP - 910

JO - Diabetes Reviews

JF - Diabetes Reviews

SN - 1935-5548

IS - 6

ER -