Abstract 587: Inflammatory Status and Macrophage Infiltration in Relation to Insulin Resistance and Dyslipidemia among Morbid Obese Subjects

Inflammatory response and macrophage infiltration in adipocyte is associated with the development of insulin resistance status and obesity-related co-morbidities. This study is to examine the inflammatory status and macrophage infiltration in adipose tissues and their relationship with insulin resistance (IR) and dyslipidemia among morbidly obese patients.We collected blood and omental visceral fat samples from 35 morbidly obese subjects (BMI ≧ 35 kg/m 2 ) and used HOMA-IR (≧2.4) and prescription history to divide the subjects into normal and insulin resistant sub-groups. We used enzyme-linked immunosorbent assay (ELISA) to determine the advanced glycation end products (AGEs) and plasma growth arrest-specific protein 6 (GAS-6) expression levels. We used turbidimetric method to determine the concentration of high sensitivity C-reactive protein (hs-CRP) level. For adipocyte, the cluster of differentiation 68 (CD68) antibody, as macrophages infiltration of adipocyte, was determined using immunohistochemistry (IHC) methods.The mean BMI among these 35 morbidly obese subjects (20 male, 15 female) is 41.2 kg/m 2 . There are 15 subjects with normal HOMA and 20 subjects with insulin resistant HOMA. Among the IR group, the fasting glucose, insulin, triglyceride, GAS-6, CD68, levels are significantly higher than those of the normal HOMA group. CD68 level are positively correlated with fasting glucose, insulin, cholesterol and HOMA-IR level and negatively correlated with HDL-C level. After adjusting for age, gender and BMI, every increase of 1ng/mL AGEs, 1ng/mL GAS-6, 1mg/L hs-CRP, and 1μm 2 CD68 is associated with increasing of HOMA-IR by 1.323 units (p=0.030), 0.118 unit (p=0.681), 2.787 units (p=0.059), and 0.0002 unit (p=0.019), respectively.Inflammation response, especially CD68 level, is associated with the insulin resistance and dyslipidemia among the morbidly obese subjects. Additionally, it is imperative to examine the interactions between inflammation response, macrophage infiltration and inflammatory status on insulin resistance and obesity-related co-morbidities.