Avaliação dos metabólitos do óxido nítrico, inibidores endógenos da óxido nítrico sintase e homocisteína na intolerância à glicose e no diabetes / Evaluation of the nitric oxide metabolites, endogen inhibitors of nitric oxide synthase and homocystein in glucose intolerance and diabetes

RESUMO

A redução da biodisponibilidade óxido nítrico ('ANTPOT. PONTO NO') tem sido responsável por complicações vasculares em algumas doenças, incluindo Diabetes Mellitus tipo 2 (DMII). A disfunção endotelial (DE) pode ser ocasionada pela baixa biodisponibilidade do 'ANTPOT. PONTO NO' e estudos indicam que a hiperglicemia pode estar contribuindo para esse evento. Outro fato importante é que grande parte dos indivíduos que apresentam Intolerância à Glicose (IG) evolui para DMII. Portanto, o objetivo desse trabalho foi avaliar de que forma o estado hiperglicêmico poderia interferir sobre metabólitos do 'ANTPOT. PONTO NO' (S-nitrosotióis, nitrato + nitrito e nitrotirosina), inibidores endógenos da 'ANTPOT. PONTO NO'sintase (ADMA e SDMA), homocisteína e a DE através...

ABSTRACT

The nitric oxide (NO) has been responsible for vascular complications in some diseases, including Diabetes Mellitus type 2 (DMII). Endothelial dysfunction (ED) may be caused by NO low bioavailability and studies indicate that the hyperglycemia may be contributing to this event. Other important fact is that a large number of individuals who present Glucose Intolerance (GI) develop DMII. Therefore, the objective of this study was to evaluate the way the hyperglycemic state could interfere upon the NO metabolites (S-nitrosotiois, nitrate + nitrite and nitrotirosine), endogen inhibitors of NO synthase (ADMA, and SDMA) and the DE using n-acetyl-ß-glicosaminidase (NAG) activity measure. In this study, 140 volunteers participated: 12 as controls (C), 32 GI and 96 DMII. Glucose concentration was superior in GI group (109±10 mg/dL) and DMII group (165±66mg/dL) in relation to group C (88±11mg/dL) (p<0.05). Only DMII group (8,5±1.9%; 4,57±2,78mg/dL) showed high leveIs of glicade hemoglobin and frutosamine in relation to group C (6,0±0,9%; 2,31±0,27mg/dL). However, NO metabolites (nitrate + nitrite, S-nitrosotiois and nitrotirosine) showed high concentrations in groups GI (35,1±12,9µM; 137±45nM; 352±104nM) and DMII (39,2±18,OµM; 143±73nM; 472±231nM) in relation to group C (26,6±6,2µM; 78±46nM; 260±74nM). The endothelial function was aIso altered in groups GI (28,0±7,3U/L) and DMII (29,4±8,7U/L) in relation to group C (21,7±3,9U/L), as indicated by NAG activity. The same behavior was observed with endogen inhibitors of NO (ADMA and SDMA). Plasmatic homocystein concentration has not shown significant difference between the groups. Data has shown that the individuaIs IG presented biochemistry alterations, related to the oxidative stress and the endothelial dysfunction, similar to the patients with DMII, which could contribute to the development of cardiovascular diseases.