1097-P: Association between Adipokines and Glycemia in Children under Age 8—The PROGRESS Cohort of Mexico

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Background: The increased incidence of type 2 diabetes is closely linked to obesity, in which an accumulation of adipocytes leads to the dysregulated production of adipokines. In adults, several adipokines contribute to the development of glycemic dysregulation, however, the role of adipokines on childhood glycemia is poorly understood. We examine the longitudinal association between adipokines and glycemia using multiple timepoint data from children in Mexico City. Methods: Children from the Programming Research in Obesity, Growth, Environment, and Social Stressors (PROGRESS) cohort (948 children, 52% male) were followed longitudinally after birth. Leptin, adiponectin, glucose, and HbA1c were measured at 4, 6, and 8 years, and fasting insulin at 8 years. Adiponectin to leptin ratio (ALR) and HOMA2 (B/IR/S) indices were computed. Longitudinal association between adipokines and each of glucose and HbA1c was examined by linear mixed models. Association between adipokines and insulin and the HOMAs at age 8 was examined by multivariable linear regression. All models were adjusted for maternal and child covariates. Results: Between ages 4 and 8 years, average levels of leptin dropped from 15.7 to 13.7 ug/mL; adiponectin increased from 3.1 to 10.8 ng/mL; and ALR dropped from 9.1 to 3.1 ug/ng. Longitudinally, across timepoints 4, 6, and 8 years after birth, there was no association between adipokines and glycemia. However, the cross-sectional analysis at age 8 years found an association between leptin and insulin (1.03, 95% CI: 1.00, 1.07), HOMA2-B (1.02, 95% CI: 1.00, 1.04), HOMA2-IR (1.03, 95% CI: 1.00, 1.07), and HOMA2-S (0.97, 95% CI: 0.94, 0.99). Similar associations were observed in males and females. Conclusion: In this prepubertal cohort, leptin was associated with insulin and with HOMA indices at age 8. Further investigation is needed to understand the role of adipokines in the development of T2DM in children and the risk factors that may alter adipokine metabolism. Disclosure Y.S.Beyh: None. R.O.Wright: None. M.M.Tellez-rojo: None. A.Baccarelli: None. H.Wu: None. K.Narayan: None. L.R.Staimez: None. U.Ramakrishnan: None. M.K.Bhasin: None. M.Tolentino dolores: None. G.Estrada-gutierrez: None. M.Yitshak sade: None. Funding National Institute of Environmental Health Sciences (R01ES032242, R01ES021357, R01ES013744, P30ES009089)

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