Childhood obesity in a population at high risk for type 2 diabetes.

OBJECTIVES: To determine the prevalence of obesity and investigate its association with fasting glucose and insulin among children and adolescents in a population at high risk for type 2 diabetes. DESIGN: A cross-sectional screening survey involving anthropometry and fasting serum levels of glucose and insulin. SETTING: A remote aboriginal (Ojibwa-Cree) community in northern Manitoba, Canada. PARTICIPANTS: All children aged 4 to 19 years in the community were invited to participate, with a response rate of 82% (n = 719). MAIN OUTCOME MEASURES: Obesity is defined as body mass index exceeding the 85th percentile of the National Center for Health Statistics reference data. The diagnosis of diabetes and impaired fasting glucose is based on the new criteria of the American Diabetes Association. RESULTS: There is a high prevalence of obesity, with 64% (female) and 60% (male) exceeding the 85th percentile and 40% (female) and 34% (male) exceeding the 95th percentile. Body mass index is a significant predictor of both glucose and insulin in both sexes, independent of age. Obese children are at increased risk of being classified as having diabetes or impaired fasting glucose (odds ratio 5.1, 95% CI 1.51, 17.0). CONCLUSIONS: The early onset of type 2 diabetes in childhood is increasingly observed in many populations. Childhood obesity is a strong risk factor. Early detection and intervention directed at obesity are potential strategies to avert the long-term consequences of type 2 diabetes.

Growth hormone deficiency in patients with histiocytosis X.

Twenty-two patients with biopsy proved histiocytosis X, aged 10 months to 14 years (median 2 years) at the time of diagnosis, were observed for 6 months to 13 years (median 4 years). One patient who had received 3000 rads irradiation directly to the hypothalamic-pituitary area had clinical and biochemical evidence of growth hormone deficiency and responded to GH therapy. Thirteen patients had normal stature, normal growth velocity, and no diabetes insipidus. The GH response to insulin-induced hypoglycemia was studied in three of these 13 patients (group 1), in three children with short stature and no diabetes insipidus (group 2), and in five patients with diabetes insipidus but normal stature and growth velocity (group 3). Peak GH responses were normal (greater than 5 micrograms/L) in all patients in groups 1 and 2, but three of the five patients in group 3 had subnormal GH responses to insulin-induced hypoglycemia and to arginine, L-DOPA/propranolol, and exercise. Their growth rates continue to be normal over 6 to 14 years follow-up. Thus, although impaired GH responses were observed in four of the 12 patients tested, true growth failure occurred only in association with direct hypothalamic-pituitary irradiation. This experience and the observation that GH deficiency was diagnosed in fewer than 1% of children with histiocytosis in Canada during a 15-year period (accounting for less than 1% of all children with GH deficiency) suggest that classic GH deficiency is not a common complication of histiocytosis unless direct hypothalamic-pituitary irradiation has been given.