1647-P: High Serum YKL-40 Concentration Is Associated with One-Hour Post-Load Hyperglycemia

Abstract

Objective: Postprandial hyperglycemia is associated with oxidative stress and low-grade inflammation, which is involved in the pathogenesis of cardiovascular disease. The aim of this study was to examine whether post-load plasma glucose during oral glucose tolerance tests (OGTT) affect inflammatory biomarkers in nondiabetic subjects. Methods: We recruited 322 nondiabetic Japanese subjects including 252 with a normal glucose tolerance (NGT) and 70 with an impaired glucose tolerance (IGT). All subjects underwent OGTT and measurement of several inflammatory biomarkers. Results: No significant differences were observed in white blood cell counts, high-sensitive CRP, high-mobility group box 1 protein (HMGB1) or S100A8/A9 levels between NGT subjects with 1-h post-load plasma glucose (1h-PG) < 155 mg/dL and subjects with 1h-PG ≥ 155 mg/dL. Conversely, NGT subjects with 1h-PG ≥ 155 mg/dL exhibited higher YKL-40 levels than subjects with 1h-PG < 155mg/dL (101.6 ± 85.8 vs. 61.6 ± 53.9 ng/mL, P < 0.0001). No significant difference was observed in YKL-40 levels between NGT subjects with 1h-PG ≥ 155 mg/dL and subjects with IGT. YKL-40 levels, but not white blood cell counts, high-sensitivity CRP, HMGB1 or S100A8/A9, showed significantly positive correlations with 1h-PG (r = 0.251, P < 0.0001). Multiple regression analysis showed that YKL-40 levels were independently associated with 1h-PG, as were age, gender, alanine transaminase and systolic blood pressure. Conclusions: In nondiabetic subjects, serum YKL-40 levels correlated positively with post-load plasma glucose levels. YKL-40 is produced by several cell types such as activated macrophages, vascular smooth muscle and endothelial cells, and plays an important role in the innate immune response, angiogenesis and remodeling of extracellular matrix. Elevated YKL-40 levels related to postprandial hyperglycemia may contribute to the progression of atherosclerosis and cardiovascular events. Disclosure Y. Ikeda: None. N. Hisakawa: None. H. Takata: None. T. Ohguro: None. J. Nishiuchi: None. Y. Kumon: None.