Diabetes mellitus tipo 2 e suas complicações - associação com novos marcadores inflamatórios e moleculares

Abstract

Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes mellitus, a disease of epidemic proportions that affects millions of people worldwide. The pathogenesis of T2DM and its microvascular complications are associated with a chronic subclinical inflammation, characterized by activation of the immune system and intracellular inflammatory signaling pathways, altered expression/secretion pattern of inflammatory mediators and adipokines, endothelial dysfunction and oxidative stress. Visceral obesity plays an important role in the events that culminate in insulin resistance and T2DM. The objective of this research was to evaluate the association of biochemical and molecular inflammatory markers with T2DM, its microvascular complications and comorbidities. 102 patients with clinical and laboratory diagnosis of T2DM and 62 non-diabetic controls where selected for participation. The results indicated that T2DM patients had higher IL-6, irisin, haptoglobin, and circulating microparticles levels (platelet-, endothelial cells- and leukocytes-derived microparticles as well as tissue factor carriers); and lower endocan levels when compared to non-diabetic controls. Furthermore, visfatin levels are decreased in advanced stages of diabetic nephropathy. Body mass index, a marker of obesity status, was shown to influence in IL-6, irisin, and haptoglobin levels. IL-10 -819T/C polymorphism affected IL-10 levels in T2DM. Hp1-Hp1 genotype of the haptoglobin gene polymorphism was more frequent in the T2DM group and presented a dominant inheritance pattern. These results indicate that biochemical and cellular activation markers levels are altered in T2DM and they can be influenced by obesity status and genetic polymorphisms. Understanding how these markers influence the onset and development of T2DM may be useful to elucidate the pathogenesis mechanisms and may as well provide insights to ameliorate the clinical follow-up.