Vascular dysfunction may be a cause of diabetes and not a consequence, according to a study – Diario Siglo XXI

MADRID, 16 (EUROPE PRESS)
Scientists at the Joslin Diabetes Center (United States) have described a series of studies designed to determine the relationship between insulin, fats and the vascular system. The work, published in the scientific journal ‘Circulation Research’, has identified a new pathway in which the cells that line the blood vessels, called endothelial cells, direct the body’s metabolism. In a reversal of scientific dogma, the findings suggest that vascular dysfunction may itself be the cause of the metabolic changes that lead to diabetes, and not an effect as previously thought. Insulin resistance, one of the main risk factors for diabetes, occurs when the body’s cells do not respond to insulin and cannot use glucose (sugar) from the bloodstream. This condition is known to increase the risk of cardiovascular disease and atherosclerosis, a buildup of fats inside the vessels. blood vessels that can restrict blood flow to body tissues. The exact mechanism by which insulin and the cells lining the vascular walls act on each other is unknown.”In people with diabetes and insulin resistance, the idea has always been that white fat and inflammation cause dysfunction in blood vessels, leading to the prevalence of heart, eye, and kidney disease in this patient population. But we found that blood vessels can have an important controlling effect here, and that was not known before,” explains one of the researchers. study leaders, George King.In addition to being linked to blood vessel abnormalities, diabetes is also associated with an undesirable decrease in the body’s store of brown fat, also called brown adipose tissue. Unlike white fat, which primarily stores energy, brown fat burns energy, maintains body temperature, and regulates body weight and metabolism. In a series of experiments with a mouse model of diabetes, King and colleagues found that Engineered mice with increased insulin sensitivity only in blood vessels weighed less than control animals, even when fed a high-fat diet. It turned out that the mice with increased insulin sensitivity had more brown fat than the control animals; they also showed less damage to blood vessels. Further investigation by the team revealed that insulin signals endothelial cells in blood vessels to produce nitrous oxide, which in turn triggers the production of brown fat cells. Due to insulin resistance, endothelial cells produced less nitrous oxide (a decrease known to increase cardiovascular risk), which led to decreased production of brown fat. Because brown fat plays such an important role in regulating the body’s weight and metabolism, declining brown fat stores may be a risk factor, not a symptom, of diabetes.” What we found here is that the endothelial cells that line the blood vessels may have an important controlling effect on the amount of brown fat that develops. Nitrous oxide comes from the endothelial cells to regulate the amount of brown fat that is produced, and that finding is very exciting because in the past we thought that diabetes caused cardiovascular problems, but that relationship seems to be reversed in this scenario,” explains King. biomarkers, or signs that doctors can test for, to detect atherosclerosis or cardiovascular disease. For animal and clinical studies, this new information could open the door to an entirely new method of weight management by augmenting brown fat tissues through enhancing endothelial nitrous oxide production. “It’s all connected. We believe that blood vessels and endothelial cells play an important role not only in the regulation of brown fat, but also in the regulation of metabolism throughout the body. Thus, these endothelial cells are a key factor in weight regulation and the development of diabetes and, as other laboratories have shown, blood vessels also appear to be an important regulator of brain function. Intervening at the level of endothelial cells could have a major impact on many diseases,” says King.