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Revista Cubana de Endocrinología

versão On-line ISSN 1561-2953

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CESPEDES MIRANDA, Ela María; RIVERON FORMENT, Gretel; ALONSO RODRIGUEZ, Celia  e  CABRERA PEREZ-SANZ, Elsa. Glycemic control and oxidative damage to biomolecules observed in type 2 diabetic people. Rev Cubana Endocrinol [online]. 2014, vol.25, n.2, pp. 46-56. ISSN 1561-2953.

Introduction: poor glycemic control and lipid disorders are risk factors for vascular complications caused by diabetes mellitus. These changes are associated to oxidative stress. Objective: to analyze the lipid profile, the oxidative damage to biomolecules and the glycemic control in type 2 diabetic patients. Methods: descriptive and cross-sectional study conducted in ninety four type 2 diabetic patients. The levels of blood glucose, glycated hemoglobin, creatinine, lipid profile, tiobarbituric acid reactive substances, and of carboxyl groups as indicators of lipid peroxidation and of protein oxidation were all estimated. Data were stratified by sex, time of disease progression and glycemic control (glucose < 6.2 mmol/L vs. glucose ³ 6.2 mmol/L; glycated hemoglobin < 7 % vs. glycated hemoglobin ³ 7 %). Results: the triglyceride concentration increased in diabetics with poor glycemic control (glycated hemoglobin ³ 7 %). The tiobarbituric acid reactive substances and of carboxyl groups did not differ depending on sex and glycemic control. The levels of carboxyl groups were higher in diabetics compared to the reference values. It was confirmed that there is positive association between the tiobarbituric acid reactive substances and the time of disease progression (r= 0.271; p= 0.008) and negative association with high density lipoproteins (r= -0.449; p= 0.000). The amount of tiobarbituric acid reactive substances was higher in diabetics with 5 years of disease progression. Conclusions: the dyslipidemic phenotype was proved in diabetic patients and the oxidative damage to lipids results from the time of disease progression, regardless of sex and glycemic control.

Palavras-chave : glycemic control; oxidative damage; type 2 diabetes mellitus.

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