ABSTRACT
Cardiovascular diseases are the most common causes of morbidity and mortality in diabetic patients. Oxidative stress plays an important role in diabetic endothelial dysfunction. Under conditions of oxidative stress, free oxygen radicals may increase insulin resistance and affect pancreatic beta cells. Several experimental animal models to understand the pathogenesis of diabetes mellitus have been developed, and the model including high fat diet which leads to insulin resistance is the best animal model to mimic type 2 diabetes mellitus. In diabetes mellitus, it is well known that there is an increase in lipid peroxidation. This condition is also associated with oxidative stress. Endothelial dysfunction creates imbalance between vasoconstriction and vasodilatation. In large arteries, nitric oxide plays a main role in endothelium-dependent vasodilatation. Abnormal production or response of nitric oxide contributes vascular and endothelial dysfunction in diabetes mellitus. Oxidative stress reduces the levels of nitric oxide and diminishes endotheliumdependent vasodilatation. Therefore, in recent years, the studies to treat the diabetic complications have focused on antioxidant agents. The goal of the treatment is to decrease oxidative stress, as well as lipid and glucose levels. Thus, endothelial dysfunction may be ameliorated and diabetic vascular complications can be avoided.
Keywords:
Antioxidant, diabetes, endothelial dysfunction, oxidative stress
Introduction
Diabetes mellitus (DM) is a common chronic metabolic disease that causes disturbances in the metabolism of carbohydrates, fats, proteins and electrolytes. It can also be defined as a syndrome that is associated with chronic hyperglycemia, resulting from lack of insulin secretion from the pancreas, or lack of insulin effect (1).
Factors such as decrease in the release of insulin into the blood, reduction in the use of blood glucose and increase in production of blood glucose may cause glucose levels to remain high in DM. Considering the blood glucose level is high in DM, there is a pathology that concerns all organs and systems, especially the heart and arteries. The main cause of renal failure, adult blindness and non-traumatic lower extremity amputations is DM, according to studies conducted in developed countries (2).
In all types of DM, the main finding is hyperglycemia, but the mechanism that causes hyperglycemia is different. DM can be divided into two types: type 1 and 2 (3). Type 1 DM is characterized by a deficiency in insulin secretion and develops due to viral, toxic or autoimmune damage to the B cells of pancreas. This type is also known as juvenile DM and accounts for about 10% of all diabetic patients, and the likelihood of developing it increases in the second decade of life (4). Type 2 DM is characterized by impaired insulin secretion and peripheral target tissue resistance to insulin, and usually occurs with the loss of beta cell function. A decrease in the number of insulin receptors present in target cells may result in no response to insulin (5,6).
The classification of DM is gradually evolving with the better understanding of etiology and pathogenesis of DM. In addition to the two main types of DM; the World Health Organization has started to classify special types of DM including malnutrition-related DM, DM accompanying certain conditions and syndromes, the type along with impaired glucose tolerance and gestational DM (7). The most common type among these special types is gestational DM. This particular type is similar to type 2 DM and is related to insulin resistance. Insulin resistance develops in pregnant women due to pregnancy hormones.
In patients with diabetes, structural, biochemical and functional changes occur in tissues and organs. Acute complications can be life threatening. Long-term vascular pathologies cause loss of function in the organs. In the early stage, control of blood glucose can prevent progression of vascular complications and coronary artery disease and diabetic nephropathy can be prevented (8).
Conclusion
Endothelial dysfunction is responsible for the development of vascular complications of DM. The development of endothelial dysfunction is the result of oxidative stress and a pathological process associated with it. Reducing oxidative stress sources and antioxidant treatments can help reduce and prevent serious complications by preventing the development of endothelial dysfunction in DM. It is important to know the pathophysiological process in order to create new treatment alternatives and there is much need for both experimental and epidemiological studies.
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