Atherosclerosis in diabetes

Hunt, J. (1994). Glucose chemistry and atherosclerosis in diabetes mellitus. In Free Radicals in the Environment, Medicine and Toxicology. Current Aspects and Current Highlights (eds. H. Nohl, H. Esterbauer and C. Rice-Evans) pp. 137-162, Richelieu Press, London. 

Lyons, T.J. (1991). Oxidised low density lipoproteins a role in the pathogenesis of atherosclerosis in diabetes Diabet. Med. 8, 411-419. 

Ingestion of fenugreek powder reduces total cholesterol and triglyceride levels. Fenugreek is thus considered a dietary supplement for hyperlipidaemia and atherosclerosis in diabetic subjects (Sharma et al., 1996a). The antidiabetic effects of fenugreek seeds in type I and type II diabetes in both human and animal models have been well established (Basch et al, 2003). 

Macroangiopathy (or accelerated atherosclerosis) leads to premature coronary heart disea.se. The exact inechanisms for increa.sed susceptibility to atherosclerosis in diabetics are unknown however, hyperlipidaemia and increased protein glycation may play a role. The most common form of hyperlipidaemia observed in diabetics is hypcrtriglyceridaemia with increa.sed plasma VLDL-cholesterol and decreased HDL-choIesterol. 

M. P. Cohen, F. N. Ziyadeh, and S. Chen, Amadori-modified glycated semm proteins and accelerated atherosclerosis in diabetes Pathogenic and therapeutic imphcations, J. Lab. Clin. Med., 147 (2006) 211-219. 

Hunt, J. V., Bottoms, M. A., and Mitchinson, M. J., 1992, Ascorbic acid oxidation A potential cause of the elevated severity of atherosclerosis in diabetes mellitus, FEBS Lett. 311 161-164. 

THE RELATIONSHIP OF DIET AND ATHEROSCLEROSIS IN DIABETIC MACACA NIGRA... 

Figure 1-1. Examples ofthe two-way street connecting biochemistry and medicine. Knowledge ofthe biochemical molecules shown in the top part of the diagram has clarified our understanding ofthe diseases shown in the bottom half—and conversely, analyses ofthe diseases shown below have cast light on many areas of biochemistry. Note that sickle cell anemia is a genetic disease and that both atherosclerosis and diabetes mellitus have genetic components.

The Vascular Lesion in Diabetes 183 5.3 Free Radicals and Atherosclerosis 191... 

Nettleton JA, Steffen LM, Ni H, Liu K and Jacobs DR Jr. 2008. Dietary patterns and risk of incident type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care 31 (9) 1777—1782. 

The disturbance of balance between superoxide and nitric oxide occurs in a variety of common disease states. For example, altered endothelium-dependent vascular relaxation due to a decrease in NO formation has been shown in animal models of hypertension, diabetes, cigarette smoking, and heart failure [21]. Miller et al. [22] suggested that a chronic animal model atherosclerosis closely resembles the severity of atherosclerosis in patients. On the whole, the results obtained in humans, for example, in hypertensive patients [23] correspond well to animal experiments. It is important that endothelium-dependent vascular relaxation in patients may be improved by ascorbic acid probably through the reaction with superoxide. 

NO also reduces endothelial adhesion of monocytes and leukocytes, key features of the early development of atheromatous plaques. This effect is due to the inhibitory effect of NO on the expression of adhesion molecules on the endothelial surface. In addition, NO may act as an antioxidant, blocking the oxidation of low-density lipoproteins and thus preventing or reducing the formation of foam cells in the vascular wall. Plaque formation is also affected by NO-dependent reduction in endothelial cell permeability to lipoproteins. The importance of eNOS in cardiovascular disease is supported by experiments showing increased atherosclerosis in animals deficient in eNOS by pharmacologic inhibition. Atherosclerosis risk factors, such as smoking, hyperlipidemia, diabetes, and hypertension, are associated with decreased endothelial NO production, and thus enhance atherogenesis. 

Muis MJ, Bots ML, Bilo HJG, Hoogma RPLM, Hoekstra JBL, Grobbee DE, Stolk RP. High cumulative insulin exposure a risk factor of atherosclerosis in type 1 diabetes Atherosclerosis 2005 181 185-92. 

Primary increases of VLDL probably reflect a number of genetic determinants and are worsened by factors that increase the rate of VLDL secretion from liver, ie, obesity, alcohol, diabetes, and estrogens. A major indication for treatment is the presence of atherosclerosis in the patient or the patient s family. Treatment includes weight reduction, restriction of all types of dietary fat, and avoidance of alcohol. Fibrates or niacin usually produce further reduction in triglyceride levels if dietary measures are not sufficient. Marine omega fatty acids may also be of value. 

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