Lavjay Butani1, Madan Dharmar1, Sridevi Devaraj2, Ishwarlal Jialal3. 1. 1 Department of Pediatrics, University of California Davis Children's Hospital , Sacramento, California. 2. 2 Department of Pathology and Immunology, Baylor College of Medicine , Houston, Texas. 3. 3 Department of Pathology and Laboratory Medicine and Internal Medicine, University of California Davis , Sacramento, California.
Abstract
BACKGROUND: Higher fasting glucose and hemoglobin A1C levels are seen more often in African American (AA) and Hispanic (H) youth, even after adjusting for body mass index (BMI), pointing to other factors that might be promoting abnormal glucose tolerance, such as inflammatory mediators. Our study compared markers of inflammation and oxidative stress in adolescents of different ethnicities. METHODS: This was a cross-sectional cohort study of healthy Caucasian (C), H, and AA adolescents. Fasting urine for F2-isoprostanes and plasma for adiponectin, soluble vascular cell adhesion molecule (s-VCAM 1), interleukins (ILs), and tumor necrosis factor-α were collected and analyzed. Insulin resistance was measured by homeostasis model assessment of insulin resistance (HOMA-IR). Multivariable regression analyses were used to assess the effect of the biomarkers on HOMA-IR. RESULTS: Seventy adolescents were enrolled (26 C, 20 A, and 24 H); 32 were male (46%) and 27 (39%) were obese. Exploratory analysis showed that for every 1 U increase in BMI z-score, IL-8 rose by 0.53 (0.05, 1.00), P = 0.03. On regression analyses, for every unit increase in BMI z-score, HOMA-IR increased by 0.67 U (P = 0.001); for every unit increase in IL-8, HOMA-IR decreased by 0.21 U (P = 0.04). None of the other biomarkers was significantly associated with HOMA-IR. CONCLUSIONS: Higher insulin resistance was associated with increasing BMI z-scores and lower IL-8. This pilot study demonstrates the need to further evaluate inflammatory markers as an independent risk factor for the development of diabetes and to explore if there is a cause and effect relationship between IL-8 and insulin resistance. This could prove valuable for early identification of insulin resistance and as targets for intervention.
BACKGROUND: Higher fasting glucose and hemoglobin A1C levels are seen more often in African American (AA) and Hispanic (H) youth, even after adjusting for body mass index (BMI), pointing to other factors that might be promoting abnormal glucose tolerance, such as inflammatory mediators. Our study compared markers of inflammation and oxidative stress in adolescents of different ethnicities. METHODS: This was a cross-sectional cohort study of healthy Caucasian (C), H, and AA adolescents. Fasting urine for F2-isoprostanes and plasma for adiponectin, soluble vascular cell adhesion molecule (s-VCAM 1), interleukins (ILs), and tumor necrosis factor-α were collected and analyzed. Insulin resistance was measured by homeostasis model assessment of insulin resistance (HOMA-IR). Multivariable regression analyses were used to assess the effect of the biomarkers on HOMA-IR. RESULTS: Seventy adolescents were enrolled (26 C, 20 A, and 24 H); 32 were male (46%) and 27 (39%) were obese. Exploratory analysis showed that for every 1 U increase in BMI z-score, IL-8 rose by 0.53 (0.05, 1.00), P = 0.03. On regression analyses, for every unit increase in BMI z-score, HOMA-IR increased by 0.67 U (P = 0.001); for every unit increase in IL-8, HOMA-IR decreased by 0.21 U (P = 0.04). None of the other biomarkers was significantly associated with HOMA-IR. CONCLUSIONS: Higher insulin resistance was associated with increasing BMI z-scores and lower IL-8. This pilot study demonstrates the need to further evaluate inflammatory markers as an independent risk factor for the development of diabetes and to explore if there is a cause and effect relationship between IL-8 and insulin resistance. This could prove valuable for early identification of insulin resistance and as targets for intervention.