GLYCERALDEHYDE-DERIVED ADVANCED GLYCATION END PRODUCTS DECREASE WHITE ADIPOSE TISSUE WEIGHT AND DOWNREGULATE LEPTIN, ADIPONECTIN, AND MACROPHAGE MARKER.

摘要

Metabolic syndrome is the coexistence of several risk factors for arteriosclerosis, including visceral obesity, hyperglycemia, dyslipidemia, and hypertension. Among these factors, obesity has been thought the most important determinant for metabolic syndrome. Obesity is marked by the expansion of white adipose tissue which induces the defective secretion of adipocytokines, inflammation, and oxidative stress, which cumulatively lead to development and progression of insulin resistance. Recently, it was reported that glucose-, glyceraldehyde(GLA)-, and glycolaldehyde-derived advanced glycation end products (AGEs) induce generation of intracellular ROS, and then contribute to inhibition the differentiation to adipocytes, attenuation of insulin sensitivity, and upregulation of monocyte chemoattractant protein-1 (MCP-1) in 3T3-Ll cells. However, it is not clear whether AGEs alter function of adipose tissue in vivo. In this study, we examine the effects of GLA-BSA on white adipose tissuess accumulation as well as the expression of adipocytokines and markers of inflammation.