Maternal and Sex Dependency of Insulin Resistance: Longitudinal PET and Echocardiography Study from the Healthy Fetus to the Adult Minipig

Cardiovascular disease is the foremost cause of mortality in the world. Among predisposing factors, obesity and metabolic syndrome are growing in prevalence. The pathogenesis of these disorders and of their complications is closely related to insulin resistance, promoting hyperglycemia and dyslipidemia through the loss of insulin action in the liver, skeletal muscle, and adipose tissue. The occurrence of insulin resistance in the myocardium is considered a sign of cardiovascular vulnerability (1,2), reflecting the inability of the heart to switch from the use of fatty acids to that of glucose, which is an oxygen-sparing (i.e., more efficient) substrate. The recent state of knowledge supports the role of oxidative stress in translating these metabolic abnormalities into organ dysfunction. The oxidant pathway is stimulated by insulin resistance and metabolic syndrome–related features, and DNA oxidative damage in peripheral blood cells has been reported in association with these conditions and with heart disease of various origins