Repositori URV

Identificador: TDX:527

Handle: https://hdl.handle.net/20.500.11797/TDX527

Autores:
Broch i Montané, Montserrat

Resumen:
Type 2 diabetes mellitus (DM2) was caused basically by the reduction of the insulin action (insulin resistance) and by the deterioration of the beta cells function. The DM2 and obesity are intimately related between them. In this way, the adipose tissue is able to synthesize and secrete various molecules that are related to the insulin sensitivity (Si) modulation such as Tumor Necrosis Factor-alfa (TNF) and interleukin-6 (IL-6).TNF- signals thorough at least two known cell-surface receptors: TNFR1 and TNFR2. The joining of the cytokine to their receptors derived to receptors soluble forms (sTNFR1 and sTNFR2). 'In vivo' studies, cytokine supply could inhibit the insulin-stimulated glucose uptake. In genetic fat and /or diabetics animals there is an over-expression of this cytokine in fat tissue and in plasma.In obese patients, there is an over-expression of TNF and TNFR2 in fat tissue and of sTNFR2 in plasma. These over-expressions are related to the body mass index and insulin levels, both markers of insulin resistance.On the other hand, the IL-6 induces to hypertrygliceridemia 'in vivo' and 'in vitro'.In humans, this cytokine is over-expressed in obese and DM2 patients and it is involved in the classical insulin resistance markers. G-allele of the -174G>C polymorphism has been found to be associated with elevated transcription rates.The goals of the presented studies are to analyse TNF system and IL-6 and their relation to insulin sensitivity.1. Plasma levels of the soluble fraction of tumor necrosis factor receptor 2 and insulin resistance. Diabetes, 47:1757-62, 1998Obese patients (BMI >30 < 40 kg/m2) showed increased plasma levels of sTNFR2 in comparison with lean. These levels are correlated positively with BMI, fat free mass and gluc