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Late Reactive Hypoglycemia as a Sign of Early Glycemic Dysfunction in Obese Adolescent Girls
Antonia Ekerdt1, Anne-Marie Carreau1, Yesenia Garcia-Reyes1, Haseeb Rahat1, Laura Pyle1, K.J. Nadeau1, 2, Melanie Cree-Green1, 2. 1Pediatric Endocrinology, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado, United States, 2Center for Women's Health Research, University of Colorado Denver, Aurora, Colorado, United States

Purpose of Study The combination of obesity and adolescence increases risk of insulin resistance and dysglycemia. Idiopathic reactive hypoglycemia (RHG) has been observed to be common in adult populations with obesity, but its mechanisms and prevalence are not well understood in adolescent populations, particularly in females at higher risk for dysglycemia. Thus our goals were to document rates of RHG in a group of adolescent girls with obesity and to identify markers associated with RHG.
Methods Used 98 sedentary adolescents with obesity (12-21 years; BMI>90th %ile for age and gender) were enrolled. Participants taking medications altering glucose metabolism or regulated hormones were excluded. After a 12 hour monitored fast and baseline metabolic and hormonal labs, girls were administered a 6 hour oral sugar tolerance test (OSTT) of 75 g glucose and 25 g fructose and indices of glucose metabolism were measured. MRI for visceral and hepatic fat was performed. Glycemia was categorized as follows: blood glucose (BG)≥70 mg/dL normoglycemic; 69 mg/dL≥BG≥62 mg/dL indeterminate and were excluded from analysis; BG≤61 mg/dL RHG. Normoglycemic and RGH group demographics, metabolic labs and OSTT area under the curves were compared with t-test or Mann-Whitney. OSTT curves were also compared with two-way ANOVA with repeated measures.
Summary of Results Of the total cohort, 16% of girls had RGH and 35% had normoglycemia. The mean time for RHG was 240 min post OSTT drink. The AUC of insulin and glucose in the first 3 hours was higher in RHG group (p = 0.04 for both). 42% of participants with RHG had impaired glucose tolerance. RHG had higher amounts of visceral fat and a higher waist-to-hip ratio (p = 0.04 for both) compared to normoglycemia and a high rate of familial history of type 2 diabetes (81%).
Conclusions RHG was relatively common in this population. RHG is associated with classic metabolic risk factors of central obesity and hyperglycemia as well as high family history of type 2 diabetes. Further studies should be conducted to understand the long-term effects and outcomes of RHG and its prediction for the development of type 2 diabetes.


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