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Published on: November 13, 2016
Glucagon stimulation test as a possible predictor of residual β-cell function
Kei Yoshida1, Tatsuhiko Urakami1, Ichiro Morioka1
1Department of Pediatrics and Child Health, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Japan.
Insights
Early glucagon stimulation tests (GST) in Japanese children with type 1 diabetes (T1D) can predict remaining beta-cell function. Peak C-peptide levels on GST help forecast the decline of this function over time.
Area of Science:
- Endocrinology
- Pediatrics
- Diabetes Research
Background:
- Type 1 diabetes (T1D) management requires understanding residual beta-cell function.
- Predictive markers for beta-cell function decline are crucial for T1D prognosis.
Purpose of the Study:
- To evaluate the predictive value of C-peptide levels from glucagon stimulation tests (GST) in Japanese children with new-onset T1D.
- To assess the long-term residual beta-cell function in relation to early GST results.
Main Methods:
- Retrospective study of 65 Japanese children with new-onset T1D (age <16 years).
- Glucagon stimulation test (GST) performed within one month of diagnosis.
- Postprandial serum C-peptide levels measured at multiple time points up to 120 months post-diagnosis.
Main Results:
- Specific peak serum C-peptide cutoff values on GST predicted beta-cell destruction at various time points (3-60 months).
- For instance, a cutoff of 0.20 ng/mL predicted beta-cell destruction at 3, 6, and 12 months.
- Multivariate analysis identified peak C-peptide, diabetic ketoacidosis, age, and HbA1c at diagnosis as predictors of residual beta-cell function.
Conclusions:
- Early GST C-peptide levels in Japanese children with T1D are significant predictors of residual beta-cell function.
- These findings can help forecast the rate of beta-cell function decline over time.
Background:
We aimed to investigate the significance of the C-peptide levels on a glucagon stimulation test (GST) conducted soon after diagnosis as a predictive marker for residual β-cell function over time in Japanese children with type 1 diabetes (TD1).
Methods:
We retrospectively enrolled 65 Japanese children (25 male, 40 female; age <16 years) with new-onset TD1. A GST was conducted within 1 month of diagnosis, when glucose toxicity improved. One- to 2-h postprandial serum C-peptide values were measured at 0, 3, 6, 12, 24, 36, 60, and 120 months after diagnosis.
Results:
Receiver operating characteristic analysis showed that the cutoff values of peak serum C-peptide levels used to predict the complete destruction of β-cells at 3, 6, and 12 months after diagnosis were all 0.20 ng/mL (area under the curve [AUC] 0.867, 95% confidence interval [CI] 0.745-0.990; AUC 0.774, 95% CI 0.634-0.914; and AUC 0.804, 95% CI 0.695-0.914, respectively); the values at 24, 36, and 60 months were 0.69 ng/mL (AUC 0.828, 95% CI 0.721-0.936), 0.60 ng/mL (AUC 0.777, 95% CI 0.636-0.918), and 0.70 ng/mL (AUC 0.848, 95% CI 0.715-0.982), respectively. On multivariate analysis, peak serum C-peptide level on a GST, diabetic ketoacidosis, age, and HbA1c level at diagnosis were associated with residual β-cell function over time.
Conclusions:
Peak serum C-peptide levels on a GST conducted soon after diagnosis in Japanese children with TD1 could predict the time to decrease in postprandial serum C-peptide values to < 0.20 ng/mL.
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