Author(s): Serrano Rios M
Abstract Share this page
Abstract Obesity and non-insulin-dependent diabetes mellitus (NIDDM) are closely linked. They frequently occur together in patients, and body mass index (BMI) is the strongest risk factor for the development of NIDDM. Both obesity and NIDDM are also major causes of morbidity and mortality from atherogenic macrovascular disease, and they are independent risk factors for coronary heart disease. The risk of developing NIDDM and cardiovascular disease is affected by the regional distribution of body fat. Visceral obesity is associated with a higher degree of risk than peripheral obesity. The metabolic and circulatory changes associated with visceral obesity lead to the development of insulin resistance and increased lipoprotein synthesis. For example, the change in the population profile of lipoproteins in the blood, and alterations in the levels of oxidative stress lead to an increased cardiovascular and macrovascular risk. The changes in lipid metabolism also affect haemorrheological function. They have been linked to decreased fibrinolysis (a serious cardiovascular risk factor) through elevated levels of plasminogen activator inhibitor factor, high blood viscosity, and increased erythrocyte aggregability. Increased BMI also appears to be associated with endothelial dysfunction, which is a major factor in atheroma plaque formation and development of thrombosis. Visceral obesity therefore adds a significant burden to the already increased cardiovascular risk inherent in NIDDM. However, even moderate weight loss may successfully reverse the majority of changes seen with visceral obesity.
This article was published in Eur J Clin Invest
and referenced in Journal of Diabetes & Metabolism