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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 한국식품영양과학회 Journal of Food Science and Nutrition Journal of Food Science and Nutrition Vol.1 No.1
- 발행연도
- 1996.6
- 수록면
- 134 - 142 (9page)
이용수
초록· 키워드
오류제보하기
Diabetes carries an increased risk of atherosclerotic disease that is not fully explained by known cardiovascular risk factors. There is accumulating evidence that advanced glycation of structural proteins, and oxidation and glycation of circulating lipoproteins, are implicated in the pathogenesis of diabetic atherosclerosis. Reactions involving glycation and oxidation of proteins and lipids are believed to contribute to atherogenesis. Glycation, the nonenzymatic binding of glucose to protein molecules, can increase the atherogenic potential of certain plasma constituents, including low density lipoprotein(LDL). Glycation of LDL is significant increased in diabetic patients compared with normal subjects, even in the presence of good glycemic control. Metabolic abnormalities associated with glycation of LDL include diminished recognition of LDL by the classic LDL receptor ; increased covalent binding of LDL in vessel walls ; enhanced uptake of LDL by macrophages, thus stimulating foam cell formation ; increased platelet aggregation ; formation of LDL-immune complexes ; and generation of oxygen free radicals, resulting in oxidative damage to both the lipid and protein components of LDL and to any nearby macromolecules. Oxidized lipoproteins are characterized by cytotoxicity, potent stimulation of foam cell formation by macrophages, and procoagulant effects. Combined glycation and oxidation, “glycoxidation” occurs when oxidative reactions affect the initial products of glycation, and results in irreversible structural alterations of proteins. Glycoxidation is of greatest significance in long lived proteins such as collagen. In these proteins, glycoxidation products, believed to be atherogenic, accumulate with advancing age : in diabetes, their rate of accumulate is accelerated. Inhibition of glycation, oxidation and glycoxidation may form the basis of future anti atherogenic strategies in both diabetic and nondiabetic individuals.
목차
Abstract
INTRODUCTION
DYSLIPIDEMIA IN DIABETES
GLYCATION OF LIPOPROTEINS
GLYCATION AND GLYCOXIDATION
GLYCATION AND OXIDATION OF LDL
LDL GLYCATION
LDL GLYCOXIDATION
GLYCATION OF CIRCULATING LIPOPROTEINS IN DIABETES
ADVANCED GLYCATION AND ATHEROSCLEROSIS
CONCLUSION
REFERENCES
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