Type 2 diabetes mellitus in African-American adolescents: Impaired beta-cell function in the face of severe insulin resistance

Doris Taha, Vatcharapan Umpaichitra, Mary Ann Banerji, Salvador Castells

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


We have previously demonstrated abnormalities in insulin secretion in adolescents with type 2 diabetes mellitus (DM2) in response to the mixed meal test and to glucagon. In order to further assess beta-cell function in DM2, we measured insulin and C-peptide responses to oral glucose in adolescents with DM2 in comparison to non-diabetic obese and lean adolescents. We studied 20 patients with DM2, 25 obese adolescents with matching body mass index (BMI) (33.8 ± 1.4 vs 34.3 ± 1.0 kg/m2), and 12 non-obese control adolescents (BMI 22.6 ± 0.6 kg/m2). Mean age, sex and sexual maturation did not differ between the three groups. All adolescents with DM2 had negative islet cell antibodies (ICA); five patients were on diet and 15 on insulin treatment. Fasting lipid profiles were determined in all participants. Plasma glucose and serum C-peptide and insulin levels were measured at 0, 30, 60, 90, and 120 min after an oral glucose load. The C-peptide increment (ΔCP) was calculated as peak minus fasting C-peptide. Area under the curve (AUC) was estimated using the trapezoid method. Insulin resistance was estimated using the HOMA model (HOMA-IR). The first phase of insulin secretion (PH1) was computed using a previously published formula. Serum triglyceride levels were significantly higher in the patients with DM2 compared to the non-obese controls (1.4 ± 0.1 vs 0.9 ± 0.1 mmol/l; p = 0.02). Plasma glucose AUC was greater in the patients with DM2 compared to the obese and non-obese control groups (1,660 ± 130 vs 717 ± 17 vs 647 ± 14 mmol/l.min; p <0.0001). ΔCP was lower in adolescents with DM2 than in obese and non-obese adolescents (761 ± 132 vs 1,721 ± 165 vs 1,225 ± 165 pmol/l; p <0.001). Insulin AUC was lower in the patients with DM2 compared to obese controls (888 ± 206 vs 1,606 ± 166 pmol/l.h; p = 0.009), but comparable to that of the non-obese controls (888 ± 206 vs 852 ± 222 pmol/l.h; p = 0.9). Insulin AUC was also higher in the obese than in the non-obese group (p = 0.05). PH1 was significantly higher in the obese group compared to the patients with DM2 as well as to the non-obese controls (2,614 ± 2,47.9 vs 929.6 ± 403.5 vs 1,946 ± 300.6 pmol/l, respectively; p = 0.001). PH1 was also higher in the non-obese controls than in the patients with DM2 (p = 0.05). HOMA-IR was three-fold higher in the patients with DM2 than in the BMI-matched obese group, and five-fold higher than in the lean controls (14.3 ± 1.2 vs 5.4 ± 0.8 vs 2.9 ± 0.4; p = 0.0002). Adolescents with DM2 have dyslipidemia, a significant cardiovascular risk factor. Decreased beta-cell function is characteristic of adolescents with DM2 in the presence of severe insulin resistance.

Original languageEnglish
Pages (from-to)135-142
Number of pages8
JournalJournal of Pediatric Endocrinology and Metabolism
Issue number2
StatePublished - Feb 2006


  • Adolescents
  • African-American
  • Insulin resistance
  • Insulin secretion
  • Type 2 diabetes mellitus


Dive into the research topics of 'Type 2 diabetes mellitus in African-American adolescents: Impaired beta-cell function in the face of severe insulin resistance'. Together they form a unique fingerprint.

Cite this