RESUMO
Was investigated serum level of endothelial monocyte activating peptide II (EMAP-II) and endothelium-dependent dilatation in type 1 diabetes and possible relation between those. We found an increase serum level of EMAP-II and decrease of endothelium-dependent dilatation in type 1 diabetes. It was significant correlation between EMAP-II and HbAc1, blood glucose, total cholesterol, LDL, triglycerides and inverse correlation between EMAP-II and HDL, endotheliumdependent dilatation. The revealed change of EMAP-II serum level reflects an endothelial dysfunction in type 1 diabetes, alteration of carbohydrate and lipid metabolism could influence of this pathway.
Assuntos
Diabetes Mellitus Tipo 1/sangue , Dilatação Patológica/sangue , Endotélio Vascular/metabolismo , Proteínas Associadas aos Microtúbulos/sangue , Monócitos/metabolismo , Adolescente , Glicemia/metabolismo , Índice de Massa Corporal , Estudos de Casos e Controles , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Diabetes Mellitus Tipo 1/genética , Diabetes Mellitus Tipo 1/fisiopatologia , Dilatação Patológica/genética , Dilatação Patológica/fisiopatologia , Endotélio Vascular/fisiopatologia , Feminino , Expressão Gênica , Hemoglobinas/genética , Hemoglobinas/metabolismo , Humanos , Masculino , Proteínas Associadas aos Microtúbulos/genética , Monócitos/patologia , Triglicerídeos/sangue , Adulto JovemRESUMO
Endothelial dysfunction is implicated in the pathogenesis of diabetes and atherosclerosis. Endothelial monocyte-activating polypeptide-II (EMAP-II) is a multifunctional polypeptide with proinflammatory and antiangiogenic activity. EMAP-II induces procoagulant activity on the surface of endothelial cells, increases expression of E- and P-selectins and tumor necrosis factor-1, directs migration of monocytes and neutrophils, induces apoptosis in endothelial cells. The mechanisms of effects on endothelial cells, inflammatory action, anti-tumor properties, pathogenic role in diseases of the central nervous system involved in the development of the lungs during embryogenesis and pathogenic role in diseases of the lungs, in the development of cardiovascular disease.
Assuntos
Aterosclerose/metabolismo , Diabetes Mellitus/metabolismo , Endotélio Vascular/metabolismo , Proteínas Associadas aos Microtúbulos/metabolismo , Miocárdio/metabolismo , Aterosclerose/genética , Aterosclerose/patologia , Movimento Celular/efeitos dos fármacos , Diabetes Mellitus/genética , Diabetes Mellitus/patologia , Selectina E/genética , Selectina E/metabolismo , Células Endoteliais/efeitos dos fármacos , Células Endoteliais/metabolismo , Células Endoteliais/patologia , Endotélio Vascular/efeitos dos fármacos , Endotélio Vascular/patologia , Expressão Gênica , Humanos , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Proteínas Associadas aos Microtúbulos/genética , Proteínas Associadas aos Microtúbulos/farmacologia , Monócitos/efeitos dos fármacos , Monócitos/metabolismo , Monócitos/patologia , Miocárdio/patologia , Neutrófilos/efeitos dos fármacos , Neutrófilos/metabolismo , Neutrófilos/patologia , Selectina-P/genética , Selectina-P/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismoRESUMO
The atherosclerotic process begins in adolescence, and its progression is determined by the same risk factors as in adults. Endothelial monocyte activating polypeptide-II (EMAP-II) is a multifunctional cytokine with proinflammatory and antiangiogenetic activity that may play a pathogenic role in the development of endothelial dysfunction and atherosclerosis. The aim of our study was to determine the serum level of EMAP-II in childhood-onset type 1 diabetic patients and obese adolescents. We found increased of serum level of EMAP-II in childhood-onset type 1 diabetic patients and in patients with obesity that do not suffer from diabetes. Also, the level of EMAP-II correlated with the serum level of glycosylated hemoglobin and blood glucose, and key markers of lipid metabolism, body mass index. Increased serum level of EMAP-II may be one of the pathway of endothelial dysfunction in type 1 diabetes.
