Clinical Characteristics in Non-Obese Children with Type 2 Diabetes Mellitus Diagnosed by the Urine

来源 :BIT`s 2nd Annual World Congress of Endobolism-2012(2012第二届内分 | 被引量 : 0次 | 上传用户:limiao912
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  Objective: We studied clinical characteristics in non-obese children with type 2 diabetes mellitus (T2DM), which is known to be a great number in Asians compared to Caucasians.Methods: Of 266 children who were diagnosed as T2DM by the urine glucose screening program at schools in Tokyo, 28 were identified to be non-obese with % overweight <20%.Among them, 24 were eligible because they had complete information to be studied.They had neither diabetes-related autoimmunity nor genetic disorders including MODY and mitochondrial diabetes.Results: The mean age at diagnosis and at the study were 12.5±1.7 and 22.4±5.7 years.Female was dominant in gender (M/F=4/20).62.5% had T2DM in the first-and second-degree relatives.In regard with the birth weight, 20.8% was small and 8.3% was large for the gestational age.The mean levels of fasting plasma glucose (FPG) and HbA1c (NGSP) at the time of diagnosis were 133.5±86.5 mg/dL and 8.4±4.2%.The majority of the patients showed low insulin secretion capacities;i.e.the mean values of fasting insulin, HOMA-R, HOMA-β and an insulinogenic index on an OGTT were 8.2 μU/mL, 5.2 (70.8% beyond 2.5), 96.1±55.0 and 0.32 (93.3% below 0.4), respectively.Most patients were initially treated with diet and exercise therapy, after that, the majority was found to be treated with either oral hypoglycemic drugs (45.8%) or insulin (50.0%) at the time of the study.The mean duration to start the pharmacological treatment was 3.1±2.3 years.In regard with the prognosis, no patients had progressed complications.Conclusions: Characteristics of the non-obese T2DM seemed to be different from those in obese T2DM.They tended to show lower insulin secretion capacities from the time of diagnosis and earlier progress to pharmacological treatment.Some genetic factors associated with non-autoimmunity might play a role in the pathogenesis of non-obese T2DM.
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