Preserved C-peptide levels in overweight or obese compared with underweight children upon diagnosis of type 1 diabetes mellitus
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Purpose: We hypothesized that overweight or obese children might develop type 1 diabetes mellitus (T1DM) early despite residual beta-cell function. Factors independently associated with preservation of C-peptide level were analyzed. Methods: We retrospectively reviewed the medical data of 135 children aged 2.1–16.5 years with autoimmune T1DM. Body mass index (BMI), pubertal stage, and glycosylated hemoglobin (HbA1c) and C-peptide levels were evaluated. Patients were assigned to underweight (22.2%), normal weight (63.7%), and overweight or obese (14.1%) groups according to their BMI. Results: Preservation of serum C-peptide levels (≥0.6 ng/mL) was found in 43.0% of subjects. With increasing BMI, the proportions of children with preserved C-peptide levels increased from 33.3% to 41.9% to 63.2%, with marginal significance (P=0.051). Interaction analysis indicated no effect of BMI score on age at onset associated with serum C-peptide levels. The lower the C-peptide level, the younger the age of onset (P<0.001), after adjustment for BMI z-score and HbA1c level. However, no significant relationship between BMI z-score or category and onset age was evident. Upon multivariate-adjusted modeling, the odds that the C-peptide level was preserved increased by 1.2 fold (P=0.001) per year of life, by 3.1 folds (P=0.015) in children presenting without (compared to with) ketoacidosis, and by 5.0 folds (P=0.042) in overweight or obese (compared to underweight) children. Conclusion: Overweight or obese children had slightly more residual beta-cell function than did underweight children. However, we found no evidence that obesity temporally accelerates T1DM presentation.
Abstract
Purpose: We hypothesized that overweight or obese children might develop type 1 diabetes mellitus (T1DM) early despite residual beta-cell function. Factors independently associated with preservation of C-peptide level were analyzed. Methods: We retrospectively reviewed the medical data of 135 children aged 2.1–16.5 years with autoimmune T1DM. Body mass index (BMI), pubertal stage, and glycosylated hemoglobin (HbA1c) and C-peptide levels were evaluated. Patients were assigned to underweight (22.2%), normal weight (63.7%), and overweight or obese (14.1%) groups according to their BMI. Results: Preservation of serum C-peptide levels (≥0.6 ng/mL) was found in 43.0% of subjects. With increasing BMI, the proportions of children with preserved C-peptide levels increased from 33.3% to 41.9% to 63.2%, with marginal significance (P=0.051). Interaction analysis indicated no effect of BMI score on age at onset associated with serum C-peptide levels. The lower the C-peptide level, the younger the age of onset (P<0.001), after adjustment for BMI z-score and HbA1c level. However, no significant relationship between BMI z-score or category and onset age was evident. Upon multivariate-adjusted modeling, the odds that the C-peptide level was preserved increased by 1.2 fold (P=0.001) per year of life, by 3.1 folds (P=0.015) in children presenting without (compared to with) ketoacidosis, and by 5.0 folds (P=0.042) in overweight or obese (compared to underweight) children. Conclusion: Overweight or obese children had slightly more residual beta-cell function than did underweight children. However, we found no evidence that obesity temporally accelerates T1DM presentation.
참고문헌 (25)
- Donath MY, "Decreased beta-cell mass in diabetes: significance, mechanisms and therapeutic implications", Diabetologia, 47, pp.581~589 (2004)
- Libman IM, "Coexistence of type 1 and type 2 diabetes mellitus: "double" diabetes?", Pediatr Diabetes, 4, pp.110~113 (2003)
- Dahlquist G., "Can we slow the rising incidence of childhood-onset autoimmune diabetes? The overload hypothesis", Diabetologia, 49, pp.20~24 (2006)
- Naik RG, "Latent autoimmune diabetes in adults", J Clin Endocrinol Metab, 94, pp.4635~4644 (2009)
- Wilkin TJ., "Is autoimmunity or insulin resistance the primary driver of type 1 diabetes?", Curr Diab Rep, 13, pp.651~656 (2013)
- Wilkin TJ., "Diabetes: 1 and 2, or one and the same? Progress with the accelerator hypothesis", Pediatr Diabetes, 9(3Pt 2), pp.23~32 (2008)
- 문진수, "2007 한국 소아 청소년 성장도표 : 개발 과정과 전망", Korean Journal of Pediatrics, 51(1), pp.1~25 (2008), 대한소아과학회
- Mei Z, "Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents", Am J Clin Nutr, 75, pp.978~985 (2002)
- Palmer JP, "C-peptide is the appropriate outcome measure for type 1 diabetes clinical trials to preserve betacell function: report of an ADA workshop", 53, pp.250~264 (2001), Diabetes
- "Effects of age, duration and treatment of insulin-dependent diabetes mellitus on residual beta-cell function:observations during eligibility testing for the Diabetes Control and Complications Trial (DCCT)", J Clin Endocrinol Metab, 65, pp.30~36 (1987), The DCCT Research Group
- "Effect of intensive therapy on residual beta-cell function in patients with type 1 diabetes in the diabetes control and complications trial. A randomized, controlled trial", Ann Intern Med, 128, pp.517~523 (1998), The Diabetes Control and Complications Trial Research Group
- Steffes MW, "Beta-cell function and the development of diabetes-related complications in the diabetes control and complications trial", Diabetes Care, 26, pp.832~836 (2003)
- Redondo MJ, "Beta cell function and BMI in ethnically diverse children with newly diagnosed autoimmune type 1 diabetes", Pediatr Diabetes, 13, pp.564~571 (2012)
- Ludvigsson J, "Decline of C-peptide during the first year after diagnosis of Type 1 diabetes in children and adolescents", Diabetes Res Clin Pract, 100, pp.203~209 (2013)
- Cedillo M, "Obesity, islet cell autoimmunity, and cardiovascular risk factors in youth at onset of type 1autoimmune diabetes", J Clin Endocrinol Metab, 100, pp.E82~E86 (2015)
- Wilkin TJ., "The convergence of type 1 and type 2 diabetes in childhood: the accelerator hypothesis", Pediatr Diabetes, 13, pp.334~339 (2012)
- Maedler K, "Glucose induces beta-cell apoptosis via upregulation of the Fas receptor in human islets", Diabetes, 50, pp.1683~1690 (2001)
- Frayn KN., "Adipose tissue as a buffer for daily lipid flux", Diabetologia, 45, pp.1201~1210 (2002)
- Kibirige M, "Testing the accelerator hypothesis: the relationship between body mass and age at diagnosis of type 1 diabetes", Diabetes Care, 26, pp.2865~2870 (2003)
- Betts P, "Increasing body weight predicts the earlier onset of insulin-dependant diabetes in childhood: testing the 'accelerator hypothesis'(2)", Diabet Med, 22, pp.144~151 (2005)
- Knerr I, "The 'accelerator hypothesis': relationship between weight, height, body mass index and age at diagnosis in a large cohort of 9,248 German and Austrian children with type 1 diabetes mellitus", Diabetologia, 48, pp.2501~2504 (2005)
- Dabelea D, "Testing the accelerator hypothesis: body size, beta-cell function, and age at onset of type 1 (autoimmune) diabetes", Diabetes Care, 29, pp.290~294 (2006)
- Greenbaum CJ, "Preservation of betacell function in autoantibody-positive youth with diabetes", Diabetes Care, 32, pp.1839~1844 (2009)
- Sochett EB, "Factors affecting and patterns of residual insulin secretion during the first year of type 1 (insulin-dependent) diabetes mellitus in children", Diabetologia, 30, pp.453~459 (1987)
- Donga E, "Insulin resistance in patients with type 1 diabetes assessed by glucose clamp studies: systematic review and meta-analysis", Eur J Endocrinol, 173, pp.101~109 (2015)