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L Fábryová

Publications and source records attributed to L Fábryová.

7 recordsLinked to original sources
PubMed1995

[Free oxygen radicals in atherosclerosis and diabetes mellitus].

Recent research suggests that reactive oxygen species (including free radicals) may be involved in the initiation and development of vascular complication in diabetics. Free radicals meet many of the criteria required for a role in the pathogenesis of diabetic vascular disease: they are present in tissues affected by the diabetic process, they have a direct toxic effect on tissues, under certain condition glucose molecules can induce free radicals production. Diabetes mellitus represents a state of increased oxidative stress which is based on evidence of increased peroxidation, glycoxidation and reduced antioxidant reserve. Glycative stress can be modified by reducing glycemia, maintaining good diabetic control, and identifying the patients in whom diabetes or impaired glucose tolerance has not been diagnosed. Strategies for reducing the oxidative stress may include the supplementation of antioxidant micronutrients (vitamins E and C, beta-carotene). At present the most appropriate dose, form, method and site of administration of antioxidants are not known. One interesting therapeutic approach for the future will be to make apo-B particles more resistant to oxidative modification or to reduce the prooxidant activity in general.

Arteriosclerosis↗
PubMedDate not supplied

[Relation between insulin resistance and small, dense lipoproteins with low density and the development of atherosclerosis in type 2 diabetes mellitus].

Diabetes mellitus type 2 (DM type 2) is a common disease that is associated with high mortality and morbidity due to macrovascular and microvascular complications. CHD mortality and morbidity is 2-3 times higher in diabetic than in non-diabetic patients. There are many potentially atherogenic factors in diabetes these may underlie this problems. Except major risk factors (high serum cholesterol concentration, hypertension, cigarette smoking), insulin resistance is common in DM type 2 patients. The dyslipidemic component of insulin resistance is "atherogenic lipoprotein phenotype", its components include small LDL particles (pattern B) with higher atherogenic risk. Several recent studies have demonstrated the preponderance of small, dense LDL in patients with DM type 2 and IR. The question of whether small, dense LDL can be explained by triglyceride levels alone or whether it is directly related to DM type 2 and insulin resistance is still the subject of debate. If serum triglycerides exceed 1.3 mmol/l, small, dense LDL increases. The practical implication is that serum triglyceride levels should be maintained as low as possible to prevent the deleterious effects of triglycerides on LDL subclass distribution and size. There are several potential mechanisms to explain the increased atherogenicity of dense LDL (small dense LDL is more susceptible to lipid peroxidation and oxidation leading to its increased uptake by macrophages and subsequent removal by scavenger pathway, also has a lower binding affinity to LDL receptors). Theoretical grounds postulate that the treating of diabetic dyslipoproteinemias would reduce atherosclerosis disease. However, to date, there have been no intervention studies specifically designed to test this postulate in the diabetic population. Such studies the Diabetes Atherosclerosis Intervention Study (DAIS), Fenofibrate Intervention and Event Lowering in Diabetes (FIELD), Collaborative Atorvastatin in Diabetes Study and Lipid in Diabetes Study are currently in progress. (Tab. 4, Fig. 2, Ref. 81.)

Arteriosclerosis↗