No abstract

The aim of the present study was to examine the effects of obesity alone and obesity associated with Type 2 diabetes on the structure, vascular reactivity and response to insulin of isolated human subcutaneous fat arterioles; these effects were correlated with the expression of insulin signalling proteins. Periumbilical subcutaneous adipose tissue was explanted during surgery, small arterioles (internal diameter 220 ± 40 μm) were dissected out and investigated by electron microscopy, myography and immunoblotting. Compared with the subcutaneous arterioles of lean subjects, obesity activated the endothelium, enhanced the accumulation of collagen within vascular wall and increased the sensitivity of adrenergic response; obesity also diminished eNOS (endothelial NO synthase) protein expression, NO production, and endothelium-dependent and insulin-induced vasodilatation, as well as the protein expression of both IRS (insulin receptor substrates)-1 and IRS-2 and of the downstream molecules in the insulin signalling pathway, such as PI3K (phosphoinositide 3-kinase), phospho-Akt and Akt. When obesity was associated with Type 2 diabetes, these changes were significantly augmented. In conclusion, obesity alone or obesity associated with Type 2 diabetes alters human periumbilical adipose tissue arterioles in terms of structure, function and biochemsitry, including diminished eNOS expression and reduced levels of IRS-1, IRS-2, PI3K and Akt in the insulin signalling pathway.

Our results support the notion that increasing the number of circulating endothelial progenitor cells by different ways could be a promising therapeutic tool for atherosclerosis.

Sepsis is a clinical syndrome defined by the presence of infection and systemic inflammatory response to infection and results from a complex interaction between the host and infectious agents. It is characterized by the activation of multiple inflammatory pathways, with an increased risk of mortality. The incidence of sepsis has been on an ever-increasing pathway in recent years. Sepsis can be induced by several clinical situations that predispose to its occurrence: malignant tumors, organ transplantation, AIDS, radiation therapy, burns, sores, polytrauma, diabetes mellitus, hepatic failure, renal failure, malnutrition, catheters or different invasive devices, and urinary catheters. The microorganisms involved in the pathogenesis of sepsis are Gram-positive cocci ( Staphylococci , Streptococci ) and Gram-negative bacilli ( Klebsiella, Pseudomonas aeruginosa , E. coli ), fungi ( Candida ), parasites, and viruses. Among mechanisms involved in septic shock production, two pathological phenomena appear: the profound decompensation of circulation and metabolic disturbances that evolve towards an irreversible state. The intimate mechanism of shock involves the activation of monocytes, macrophages and neutrophils by lipopolysaccharides of Gram-negative bacteria. The microvascular bed is directly involved in the etiopathogenesis of disorders of acute inflammatory states associated with or without sepsis. A better comprehension of sepsis pathophysiology, especially the molecular mechanisms of septic shock, allows for new therapeutic perspectives.

Cardiovascular diseases (CVD) are the main object of morbidity and death in the world. There are different triggers of CVD, but atherosclerosis and/or hypertension are the most usual. CVD risk factors are used as prognosticators of disease process, while the biomarkers that envisage cardiovascular risk have an important biological basis. The integration of CVD risk factors and new biomarkers can improve CVD risk stratification and disease management. The identification of microparticles (MPs) in body fluids has opened new perspectives in diagnosis, prognosis and therapy of CVD pathogenesis. MPs are submicron vesicles released from a diversity of cell types with pleiotropic biological effects on signaling among cells. They are correlated with disease state and play a major role in atherosclerosis associated with inflammation, thrombosis as well as in CVD development and progression. This review reveals many sides of MPs as risk factors, biomarkers, novel forms of intercellular communication, non-invasive potential diagnostic tools and discusses their positive and negative impact on CVD.