Do obese youth recover insulin sensitivity similarly to lean youth at the end of puberty? The Health in Puberty (HIP) Study
Ergui, Ian   (University of Colorado at Denver and Health Sciences Center)
Mentor: Kelsey, Megan (University of Colorado)
The prevalence of type 2 diabetes in the pediatric population has seen a significant increase in the past twenty years1,2. The easy availability of energy rich nutrition and the rise in sedentary behaviors in youth may be responsible for this increase in pediatric type 2 diabetes (T2DM)3,4. The pubertal period represents a time of especially high risk for T2DM: insulin sensitivity decreases precipitously over the course of puberty and then returns to pre-pubertal levels at the conclusion of puberty5. Overweight youth are subjected to especially high risk at the onset of puberty as they are more insulin insensitive at baseline as compared to their lean peers. Cross sectional hyperinsulinemic-euglycemic clamp studies have indicated that insulin sensitivity reaches its lowest point at Tanner Stage 3-4 but more research is needed to assess whether obese youth fail to recover a similar degree of insulin sensitivity to that of their lean peers. The Health Influences in Puberty Study (HIP) was a single center longitudinal study comparing changes in insulin sensitivity and secretion in obese versus normal weight youth during puberty. The aim of the study was to compare the differences in insulin sensitivity, insulin secretion and disposition index (DI, a measure of ß cell function in relation to insulin sensitivity) in lean and obese youth as they progress from early to late puberty. The hypotheses were: 1) insulin sensitivity fails to recover during puberty in obese youth in comparison to their lean counterparts and 2) DI decreases more significantly during puberty in obese youth compared to lean youth. For this analysis, 50 youth aged 9 years or older and Tanner 2 or 3 were studied. Lean participants (n=33) had BMIs = 5th percentile and = 85th percentile while obese participants (n=17) had BMIs = 95th percentile. Participants did not have a history of type 2 diabetes or impaired glucose tolerance at the time of enrollment. Participants underwent intravenous glucose tolerance testing (IVGTT) at baseline and again at Tanner stage 5 of development. No significant differences were observed in insulin sensitivity (lean -2.47}6.8, obese -1.15}3.33, p=0.36), insulin secretion (lean 119.06}408.11, obese 70.32}1162.32, p=0.87) or DI (lean - 484.74}2140.69, obese -1651.79}2821.75, p=0.15) over the course of puberty. In obese participants insulin sensitivity was lower at baseline, insulin secretion was elevated at all time points and DI decreased more than in lean participants. Both lean and obese participants failed to recover prepubertal levels of insulin sensitivity at the early Tanner 5 stage of development. Insulin sensitivity, secretion and DI are impacted both by obesity and puberty. Further studies are needed to understand the natural trajectory of insulin sensitivity and secretion after puberty has ended and whether puberty negatively impacts ß cell function in obese youth.