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Resumen de Resistencia insulínica y otras expresiones del síndrome metabólico en niños obesos chilenos

Salesa Barja, Antonio Arteaga Ll, Ana M Acosta B, María Isabel Hodgson

  • Background: Infantile obesity is a probable risk factor for the early appearance of chronic illnesses like Type 2 Diabetes Mellitus, Dislipidemia and Hypertension. Insulin Resistance (IR) appears as the common etiological mechanism. Aim: To describe metabolic complications associated to obesity in a group of Chilean children and to correlate them with IR, estimated through the homeostasis model assessment index (HOMA). Subjects and methods: We studied 88 children, 12±2.4 years old. Fifty two had severe obesity, 19 were overweight, and 17 had a normal weight (body mass index z score (BMIz): 4.7±1.6, 1.7±0.5 and 0.2±0.6 respectively, p <0.001). In obese children, an oral glucose tolerance test, measuring basal and 30 min insulin levels, was performed and serum lipid levels were measured. Results: Eleven percent of the severely obese children were glucose intolerant, 67% had basal hyperinsulinemia (>20 uU/ml) and 79% had IR (HOMA >3.8). These children also had a higher prevalence of acantosis nigricans than the overweight and normal counterparts (63, 10.5 and 0% respectively, p <0.001), higher basal insulinemia: (24.4±10, 16.4±4 and 12.2±3 mU/ml respectively) and HOMA (5.3±2, 3.4±0.8 and 2.3±0.5 respectively, p <0.001). By multiple stepwise regression analysis, BMIz was the only significant predictor for basal hyperinsulinemia, HOMA and diastolic blood pressure. Age and BMIz were independent predictors for systolic blood pressure. The strongest predictor for plasma lipid levels was the family history of dislipidemia. Conclusions: Obese children have a high prevalence of metabolic complications, which are related to the severity of obesity. Most of the severely obese children have hyperinsulinism and IR. BMIz is the principal predictor for high blood pressure. Familiar history is the better predictor for dislipidemia (Rev Méd Chile 2003; 131: 259-68).


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