Skip to main content
ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #294451
Title: Progressive deterioration of beta-cell function in obese youth with type 2 diabetes

Author
item BACHA, FIDA - Children'S Nutrition Research Center (CNRC)
item GUNGOR, NESLIHAN - Louisiana State University
item LEE, SOJUNG - University Of Pittsburgh Medical Center
item ARSLANIAN, SILVA - University Of Pittsburgh Medical Center

Submitted to: Pediatric Diabetes
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/5/2012
Publication Date: 3/1/2013
Citation: Bacha, F., Gungor, N., Lee, S., Arslanian, S.A. 2013. Progressive deterioration of beta-cell function in obese youth with type 2 diabetes. Pediatric Diabetes. 14(2):106-111.

Interpretive Summary: In adults, type 2 diabetes (T2DM) is characterized with progressive deterioration in insulin production. Data are scanty in youth. We investigated the change in beta-cell function (reflective of insulin production by the pancreas beta cells) in youth with T2DM. Six adolescents with type 2 diabetes underwent evaluation within 3 years of the diagnosis of diabetes and after 12-16 months of follow-up. We found that the rate of decline in beta-cell function was approximately 20% per year. This rate indicates more rapid deterioration in the function of the beta cells in children with type 2 diabetes. Interventions to retard this deterioration should be investigated.

Technical Abstract: In adults, type 2 diabetes (T2DM) is characterized with progressive deterioration in insulin secretion. Data are scanty in youth. We investigated prospectively the change in ß-cell function and in insulin sensitivity in youth with T2DM. Six adolescents with T2DM [hemoglobin A1c (HbA1c) 6.6 +/- 1.0%] underwent evaluation of hepatic glucose production (HGP; [6,6-2H2] glucose), insulin-stimulated glucose disposal (Rd; hyperinsulinemic-euglycemic clamp), first- and second-phase insulin/C-peptide secretion (hyperglycemic clamp), body composition dual energy X-ray absorptiometry (DEXA), and abdominal adiposity (computed tomography) within 3 yr of the diagnosis of diabetes and after 12–16 months of follow-up. Weight, body mass index (37.1 +/- 6.9), HbA1c (6.3 +/- 0.7%), HGP (2.8 +/-1.2 mg/kg/min), and Rd (4.9 +/-3.4 mg/kg/min) did not change significantly from baseline. However, first-phase insulin and C-peptide declined (152.6 +/-261.2 vs. 75.9 +/- 108.5 uU/mL, p=0.028; 8.0 +/- 6.3 vs. 5.9 +/- 4.4 ng/mL, p=0.048, respectively) with no significant change in second-phase insulin/C-peptide. The rate of decline in beta-cell function was ~20% per year. After a median duration of 20 months of diabetes, youth with T2DM manifest a rapid decline in beta-cell function with no significant changes in peripheral or hepatic insulin sensitivity. Interventions to retard this deterioration in beta-cell function should be investigated.