Metabolic syndrome is a sequela of radiation exposure in hypothalamic obesity among survivors of childhood brain tumors.

Survivors of childhood brain tumors may be at risk for early onset of metabolic syndrome, possibly secondary to surgery and/or radiation exposure. This study examines effects of radiation exposure to hypothalamus-pituitary-adrenal axis (HPA) on metabolic risk among survivors of childhood brain tumors. One hundred forty-two met inclusion criteria; 60 had tumor surgery plus radiation exposure (>1 Gray (Gy)) to HPA. The second subgroup of 82 subjects had surgery only and were not exposed to radiation. Both subgroups had survived for approximately 5 years at the time of study. All had clinical evaluation, vital signs, anthropometry, measurement of body composition by dual X-ray absorptiometry and fasting laboratory assays (metabolic panel, insulin, C-peptide, insulin-like growth factor-1, leptin and adiponectin). Body composition data for both subgroups was compared with the National Health and Nutrition Survey (NHANES) subgroup of similar age, gender and body mass index. Cranial surgery was associated with obesity of similar severity in both subgroups. However, survivors exposed to radiation to the HPA also had increased visceral fat mass and high prevalence of growth hormone deficiency and metabolic syndrome. Fat mass alone did not explain the prevalence of the metabolic syndrome in radiation exposure subgroup. Other factors such as growth hormone deficiency may have contributed to metabolic risk. We conclude that prevalence of metabolic syndrome among subjects exposed to hypothalamic radiation was higher than expected from hypothalamic obesity alone. Radiation exposure may exert untoward endocrinopathies due to HPA exposure that worsens metabolic risk. Early screening for metabolic syndrome in this population is indicated.

Effects of residential summer camp on body mass index and body composition in type 1 diabetes.

BACKGROUND: Body mass index (BMI) and fat mass may be higher in children with diabetes compared to healthy peers. It is not certain how diabetic children respond to exercise and diet interventions. OBJECTIVE: To investigate the effect of summer camp on BMI and body composition in children with type 1 diabetes. METHODS: Five hundred eighty-six children (5-19 years, 518 with type 1 diabetes, 68 without diabetes) were followed while attending camp. BMI z-scores (BMIz) and body composition (bioelectrical impedance analysis) were measured at the beginning and end of each 19-day session. Diet and activity were directly supervised, blood glucose closely monitored. A nested diabetic/non-diabetic sib pair analysis was also conducted. Changes in BMIz and percent fat mass (%FM) were the primary outcomes. Findings were confirmed by analysis of data from 612 campers (549 with diabetes) the following summer. RESULTS: At entry, campers with diabetes had higher BMIz and %FM. They tended to gain BMIz (0.04 ± 0.01) whereas non-diabetic campers lost (-0.16 ± 0.11, P < .0001). BMIz increases were positively correlated with precamp hemoglobin A1c values. The differences in initial values and changes in BMIz remained when campers with diabetes were compared to their siblings. All experienced a similar reduction in %FM. Similar results were obtained the following summer. CONCLUSIONS: Children with diabetes may, therefore, accrue more lean body tissue with increased exercise and a healthy diet than those without diabetes. This effect is greatest in those with initially poor metabolic control.

Vitamin D deficiency in obese children and its relationship to glucose homeostasis.

OBJECTIVES: The aim of the study was to compare the prevalence of vitamin D deficiency in obese and non-overweight children in North Texas, to examine relationships between dietary habits and 25-hydroxyvitamin D [25(OH)D] level in obese children, and to examine the relationship between 25(OH)D level and markers of abnormal glucose metabolism and blood pressure. PATIENTS AND METHODS: Using a cross-sectional design, systolic and diastolic blood pressure, dietary information, serum 25(OH)D, fasting glucose and insulin, 2-h glucose from oral glucose tolerance test, hemoglobin A1c, and homeostasis model assessment of insulin resistance were recorded for 411 obese subjects (6-16 yr old) at an obesity referral clinic. 25(OH)D was also obtained from 87 control non-overweight subjects (6-16 yr old). RESULTS: Ninety-two percent of obese subjects had a 25(OH)D level below 75 nmol/liter, and 50% were below 50 nmol/liter. Among non-overweight subjects, these frequencies were 68 and 22%, respectively (both P < 0.01 compared with obese subjects). 25(OH)D was negatively associated with soda intake (P < 0.001), juice intake (P = 0.009), and skipping breakfast (P < 0.001). 25(OH)D was negatively correlated with homeostasis model assessment of insulin resistance (r = -0.19; P = 0.001) and 2-h glucose (r = -0.12; P = 0.04) after adjustment for body mass index and age but was not correlated with hemoglobin A1c, systolic blood pressure Z score, or diastolic blood pressure Z score. CONCLUSIONS: Vitamin D deficiency is common in children in this southern United States location and is significantly more prevalent in obese children. Lower 25(OH)D level is associated with risk factors for type 2 diabetes in obese children.

Stimulated growth hormone concentrations in obese pediatric patients with mild and severe insulin resistance: a pilot study.

BACKGROUND: GH excess predisposes to insulin resistance (IR). Obese patients have blunted responses to GH stimulation and decreased spontaneous secretion. GH secretion has not been studied in the context of IR.rr OBJECTIVE: To determine whether varying degrees of IR effects GH dynamics in obese children. PATIENTS/DESIGN: Patients (all > 10 y) were categorized according to gender and HOMA-IR to have either mild or severe IR. Twenty patients (10 female) with mild IR completed the study, as did 18 (9 female) in the severe group. Each patient underwent a GH stimulation test with GHRH. GH peak and area under the curve (AUC) were compared between the groups. RESULTS: Severe IR females had higher peak GH (mean +/- SD, 9.5 +/- 4.4 vs. 5.8 +/- 3.7 ng/dl, p = 0.04) and trended toward higher GH AUC (356 +/- 207 vs. 221 +/- 128, p = 0.06) than mild IR females. There were no differences in GH response in males, CONCLUSIONS: There may be a positive relationship between severity of IR and peak GH in obese girls.

Screening for type 2 diabetes in obese youth.

OBJECTIVE: To assess available blood tests as potential screening tools for impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). METHODS: We studied 468 obese (BMI mean: 34.4 kg/m(2)) children, including a subgroup with serum fasting insulin levels of >15 microIU/mL. Fasting laboratory tests included measurements of serum glucose and insulin, hemoglobin A1c (HbA1c), and 1,5-anhydroglucitol (insulin-resistant subgroup only) levels. An oral glucose-tolerance test was performed on each patient, and 2-hour postload serum glucose and insulin levels were obtained. Fasting blood glucose (BG), Homeostasis Model of Assessment for Insulin Resistance (HOMA-IR), HbA1c, and 1,5-anhydroglucitol values were used as predictors for exceeding various 2-hour BG cut-offs. Receiver operator characteristic curves were fitted to determine area-under-the-curve values as measures of screening efficacy. RESULTS: In the insulin-resistant subgroup, 3 (2%) patients had T2DM and 23 (12%) had IGT. Optimal sensitivity and specificity to detect T2DM were, respectively, 99% and 96% at HbA1c >or= 6.0%, and 96% and 88% at 1,5-anhydroglucitol < 17.0 microg/mL, with lower values for fasting BG and the HOMA-IR. In the entire study group, 9 (2%) patients had T2DM and 44 (9%) had IGT. Optimal sensitivity and specificity to detect T2DM were, respectively, 86% and 85% at HbA1c levels of 5.7%, 88%, and 93% at a fasting BG level of 104 mg/dL, and 62% and 70% at an HOMA-IR of 7.9. CONCLUSIONS: HbA1c, 1,5-anhydroglucitol, and fasting BG levels are good predictors of T2DM in obese children, whereas HOMA-IR values are not. HbA1c and 1,5-anhydroglucitol are excellent predictors of T2DM in insulin-resistant obese children.