Abstract
We evaluated the prevalence of glutamic acid decarboxylase autoantibody (GADA) in nonobese patients with type 2 diabetes mellitus in Korea and investigated the characteristics of GADA-positive and GADA-negative patients. Two years later, we assessed the progression of beta-cell function in these patients. Of the 647 nonobese patients with type 2 diabetes mellitus enrolled in the study, 10.1% was positive for GADA. Glutamic acid decarboxylase antibody-positive patients had lower fasting and stimulated C-peptide levels compared with GADA-negative patients (1.70 ± 0.72 vs 1.24 ± 0.59 μg/L, P < .001; 2.59 ± 1.51 vs 1.99 ± 0.82 μg/L, P < .001). Patients treated with insulin had lower fasting and stimulated C-peptide levels than those not treated (1.13 ± 0.52 vs 1.66 ± 0.73 μg/L, P = .002; 1.85 ± 0.69 vs 2.49 ± 0.91 μg/L, P = .004) and had higher titers of GADA (30.5 ± 7.3 vs 6.0 ± 4.8 U/mL, P < .001). In terms of progression of beta-cell function, fasting and stimulated C-peptide levels were significantly lower in GADA-positive patients after 2 years (from 1.24 ± 0.59 to 0.95 ± 0.54 μg/L, P = .004; from 1.99 ± 0.82 to 1.61 ± 0.77 μg/L, P = .007), whereas no such difference was observed in the GADA-negative patients. We demonstrate that a significant proportion of Korean patients may be positive for GADA; this is consistent with studies of white subjects, although disagrees with previous reports on Korean subjects. By assessing the presence of GADA in Korean type 2 diabetic patients, we are able to predict their course of beta-cell function and identify in advance those who are likely to require insulin treatment.
| Original language | English |
|---|---|
| Pages (from-to) | 1107-1112 |
| Number of pages | 6 |
| Journal | Metabolism: Clinical and Experimental |
| Volume | 55 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 2006 Aug 1 |
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All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism
- Endocrinology
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Clinical and biochemical characteristics of nonobese type 2 diabetic patients with glutamic acid decarboxylase antibody in Korea. / Kim, Chul Sik; Nam, Jae Hyun; Nam, Ji Sun; Park, Jong Suk; Kang, Eun Seok; Ahn, Chul Woo; Cha, Bong Soo; Lim, Sung Kil; Kim, Kyung Rae; Lee, Hyun Chul; Huh, Kap Bum.
In: Metabolism: Clinical and Experimental, Vol. 55, No. 8, 01.08.2006, p. 1107-1112.Research output: Contribution to journal › Article
TY - JOUR
T1 - Clinical and biochemical characteristics of nonobese type 2 diabetic patients with glutamic acid decarboxylase antibody in Korea
AU - Kim, Chul Sik
AU - Nam, Jae Hyun
AU - Nam, Ji Sun
AU - Park, Jong Suk
AU - Kang, Eun Seok
AU - Ahn, Chul Woo
AU - Cha, Bong Soo
AU - Lim, Sung Kil
AU - Kim, Kyung Rae
AU - Lee, Hyun Chul
AU - Huh, Kap Bum
PY - 2006/8/1
Y1 - 2006/8/1
N2 - We evaluated the prevalence of glutamic acid decarboxylase autoantibody (GADA) in nonobese patients with type 2 diabetes mellitus in Korea and investigated the characteristics of GADA-positive and GADA-negative patients. Two years later, we assessed the progression of beta-cell function in these patients. Of the 647 nonobese patients with type 2 diabetes mellitus enrolled in the study, 10.1% was positive for GADA. Glutamic acid decarboxylase antibody-positive patients had lower fasting and stimulated C-peptide levels compared with GADA-negative patients (1.70 ± 0.72 vs 1.24 ± 0.59 μg/L, P < .001; 2.59 ± 1.51 vs 1.99 ± 0.82 μg/L, P < .001). Patients treated with insulin had lower fasting and stimulated C-peptide levels than those not treated (1.13 ± 0.52 vs 1.66 ± 0.73 μg/L, P = .002; 1.85 ± 0.69 vs 2.49 ± 0.91 μg/L, P = .004) and had higher titers of GADA (30.5 ± 7.3 vs 6.0 ± 4.8 U/mL, P < .001). In terms of progression of beta-cell function, fasting and stimulated C-peptide levels were significantly lower in GADA-positive patients after 2 years (from 1.24 ± 0.59 to 0.95 ± 0.54 μg/L, P = .004; from 1.99 ± 0.82 to 1.61 ± 0.77 μg/L, P = .007), whereas no such difference was observed in the GADA-negative patients. We demonstrate that a significant proportion of Korean patients may be positive for GADA; this is consistent with studies of white subjects, although disagrees with previous reports on Korean subjects. By assessing the presence of GADA in Korean type 2 diabetic patients, we are able to predict their course of beta-cell function and identify in advance those who are likely to require insulin treatment.
AB - We evaluated the prevalence of glutamic acid decarboxylase autoantibody (GADA) in nonobese patients with type 2 diabetes mellitus in Korea and investigated the characteristics of GADA-positive and GADA-negative patients. Two years later, we assessed the progression of beta-cell function in these patients. Of the 647 nonobese patients with type 2 diabetes mellitus enrolled in the study, 10.1% was positive for GADA. Glutamic acid decarboxylase antibody-positive patients had lower fasting and stimulated C-peptide levels compared with GADA-negative patients (1.70 ± 0.72 vs 1.24 ± 0.59 μg/L, P < .001; 2.59 ± 1.51 vs 1.99 ± 0.82 μg/L, P < .001). Patients treated with insulin had lower fasting and stimulated C-peptide levels than those not treated (1.13 ± 0.52 vs 1.66 ± 0.73 μg/L, P = .002; 1.85 ± 0.69 vs 2.49 ± 0.91 μg/L, P = .004) and had higher titers of GADA (30.5 ± 7.3 vs 6.0 ± 4.8 U/mL, P < .001). In terms of progression of beta-cell function, fasting and stimulated C-peptide levels were significantly lower in GADA-positive patients after 2 years (from 1.24 ± 0.59 to 0.95 ± 0.54 μg/L, P = .004; from 1.99 ± 0.82 to 1.61 ± 0.77 μg/L, P = .007), whereas no such difference was observed in the GADA-negative patients. We demonstrate that a significant proportion of Korean patients may be positive for GADA; this is consistent with studies of white subjects, although disagrees with previous reports on Korean subjects. By assessing the presence of GADA in Korean type 2 diabetic patients, we are able to predict their course of beta-cell function and identify in advance those who are likely to require insulin treatment.
UR - http://www.scopus.com/inward/record.url?scp=33745826667&partnerID=8YFLogxK
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U2 - 10.1016/j.metabol.2006.04.006
DO - 10.1016/j.metabol.2006.04.006
M3 - Article
C2 - 16839848
AN - SCOPUS:33745826667
VL - 55
SP - 1107
EP - 1112
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
SN - 0026-0495
IS - 8
ER -