Cholesterol Feeding and Insulin Treatment on Lipid Peroxidation

• Main Authors: Tsai Mu-Chang, 蔡木章
• Other Authors: Su-Chien Chan
• Format: Others
• Language: zh-TW
• Published: 1998
• Online Access: http://ndltd.ncl.edu.tw/handle/91339004776893587682

碩士 === 國防醫學院 === 公共衛生學研究所 === 86 === Reactions involving glycaton and oxidation of proteins and lipids are believed to contribute to atherosclerosis. Lipid peroxidation (LPO)levels are significantly increased in diabetic patients compared with normal subjects, LPO generation is known to depend upon the action of free radicals. Recent studies shown that free radicals are generated from glycosylated proteins in the presence of a high blood glucose concentration. When lipid components in LDL are oxidized, the oxidized LDL may be taken up by macrophages and become foam cells, leading to the proliferation of smooth muscle, calcification of plaque, and accumulation of cholesterol in vascular wall, which is the early development of atherosclerosis. On the other hand, long term hyperglycemia induces glycation of protein, leads to increased formation of advanced glycation end products (AGEs), which stimulate macrophages to secret more cytokines, and in turn change the functions of both smooth muscle cells and endothelium cells of the vascular wall. AGE also change structure of collagen of arterial wall which may contribute to atherosclerosis. The purpose of this study was to examine relationship between hyperglycemia,hypercholesteremia and atherosclerosis. Hamsters were used as experimental animals in this study. The animals were divided into normal and diabetic groups, In the normal groups, hamster were fed either chow as control (N) or 0.2% cholesterol-chow and injected with saline (CS). Two groups of diabetic hamsters were injected with saline and fed either chow (DS) or 0.2% cholesterol-chow (DCS). The other two groups of diabetic hamsters were injected with insulin and fed either chow (DI) or 0.2% cholesterol-chow (DCI). After 5 weeks of treatment, all groups were sacrificed, plasma and organs of the hamsters were assayed for the levels of TBARS, carbonyl groups, AGE level, the degree of contraction and relaxation of thoracic aorta, NO level, percent of LDL glycation. The result showed that hyperglycemia resulted in increased lipid and protein oxidative stress in hamsters, and insulin treatment significantly the TBARS levels of decreased plasma, LDL, aorta and total cholesterol liver hepatic protein carbonyl groups, kidney AGE and LDL-glycation level also significantly decreased by insulin treatment, but NO level and thoracic aorta relaxation were significantly increased compared to the saline-injected diabetic hamsters. Cholesterol-feeding significantly increased oxidative damage in the normal and insulin-injected diabetic hamsters but not in the saline-injected diabetic hamsters. These result indicated that both hypercholseteremia and hyperglycemia contribute to the glycation and oxidation of proteins and lipids in the diabetic hamsters.