Similar articles

Abstract: Objective: Uncontrolled diabetes has become a major cause of mortality and morbidity by reason of vascular angiopathy. The aim of this study was to evaluate the concentrations of soluble forms of vascular adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), E-selectin, and thrombomodulin in patients with well-controlled and uncontrolled diabetes type 2. Methods: The study was conducted on 62 patients with diabetes. Group I consisted of 35 patients with well-controlled diabetes. The second group included 27 patients with uncontrolled diabetes with micro-albuminuria. A control group was made up of 25 healthy volunteers. The concentrations of sVCAM-1, sICAM-1, sE-selectin, and soluble thrombomodulin were assayed in plasma. Serum concentration of creatinine was measured and the plasma concentrations of fasting glucose and glycated hemoglobin (HbA1c) determined. Results: Lower concentrations of ICAM-1 were found in the group of uncontrolled diabetes patients compared with those with well-controlled disease. In patients with uncontrolled diabetes, VCAM-1 levels were significantly higher compared with the group with well-controlled diabetes. In patients with uncontrolled diabetes a positive correlation was obtained between glomerular filtration rate and sE-selectin and a negative correlation between the levels of creatinine and ICAM-1, although there was a positive correlation between (HbA1c) and ICAM-1. Conclusions: The study confirmed the participation of the inflammatory process associated with impaired vascular endothelial function in the pathogenesis of type 2 diabetes. The opposite effect of uncontrolled hyperglycemia on adhesion molecules suggests different functions of VCAM-1 and ICAM-1 in complications of diabetes.

未受控制的高血糖对2型糖尿病患者粘附分子的影响

[1]Booth, G., Stalker, T.J., Lefer, A.M., et al., 2002. Mechanisms of amelioration of glucose-induced endothelial dysfunction following inhibition of protein kinase C in vivo. Diabetes, 51(5):1556-1565.

[2]Bruno, C.M., Valenti, M., Bertino, G., et al., 2008. Plasma ICAM-1 and VCAM-1 levels in type 2 diabetic patients with and without microalbuminuria. Minerva. Med., 99(1):1-5.

[3]Empen, K., Frost, R.J., Geiss, H.C., et al., 2003. Differential effect of fenofibrate versus atorvastatin of E-selectin and vascular cellular adhesionmolecule-1 in patients with type 2 diabetes mellitus and mixed hyperlipoproteinemia: a randomized cross-over trial. Cardiovasc. Diabetol., 2:17.

[4]Głowińska, I., Małyszko, J., 2008. Cardiovascular complications in patients with diabetic nephropathy. Przegl. Kardiodiab., 3(3):217-222 (in Polish).

[5]Głowińska-Olszewska, B., Urban, M., Peczyńska, J., et al., 2007. Analysis of selected new biomarkers of early atherosclerosis process in children and adolescents with diabetes type 1. Przegl. Kardiodiab., 2:146-153 (in Polish).

[6]Grande, M.T., Pérez-Barriocanal, F., López-Novoa, J.M., 2010. Role of inflammation in túbulo-interstitial damage associated to obstructive nephropathy. J. Inflamm., 7(1):19.

[7]Güler, S., Cakir, B., Demirbas, B., et al., 2002. Plasma soluble intercellular adhesion molecule 1 levels are increased in type 2 diabetic patients with nephropathy. Horm. Res., 58(2):67-70.

[8]Hadi, A.R., Suwaidi, J., 2007. Endothelial dysfunction in diabetes mellitus. Vasc. Health Risk Manag., 3(6):853-876.

[9]Karalliedde, J., Gnudi, L., 2011. Endothelial factors and diabetic nephropathy. Diabetes Care, 34(Suppl. 2):S291-S296.

[10]Lu, J., Randell, E., Hun, Y., et al., 2011. Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy. Clin. Bioch., 44(4):307-311.

[11]Luis-Rodríguez, D., Martínez-Castelao, A., Górriz, J.L., et al., 2012. Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy. World J. Diabetes, 3(1):7-18.

[12]Mizia-Stec, K., Gąsior, Z., Zahorska-Markiewicz, B., et al., 2003. Immune activation in diabetes type 2 in patients with coronary artery disease. Diabetologia Doświadczalna i Kliniczna, 3(6):523-529 (in Polish).

[13]Morcos, M., Borcea, V., Isermann, B., et al., 2001. Effect of α-lipoic acid on the progression of endothelial cell damage and albuminuria in patients with diabetes mellitus: an exploratory study. Diabetes Res. Clin. Pract., 52(3):175-183.

[14]Nadar, S., Blann, A.D., Lip, G.Y., 2004. Endothelial dysfunction: methods of assessment and application to hypertension. Curr. Pharm. Des., 10(29):3591-3605.

[15]Pupek-Musialik, D., Bogdański, P., Dytfeld, J., et al., 2005. Assesment of tumor necrosis factor soluble receptor type 2 (sTNFR2) and soluble intercellular adhesion molecule 1 (sICAM-1) in obese patients with metabolic syndrome. Inflammatory process in metabolic syndrome. Endokrynol. Otył. Zaburz. Przem. Materii, 1(1):30-35 (in Polish).

[16]Salker, T.J., Skvarka, C.B., Scalia, R., 2003. A novel role for calpains in the endothelial dysfunction of hyperglycemia. FASEB J., 17(11):1511-1513.

[17]Stehouwer, C.D., Gall, M.A., Twisk, J.W., et al., 2002. Increased urinary albumin excretion, endothelial dysfunction, and chronic low-grade inflammation in type 2 diabetes: progressive, interrelated, and independently associated with risk of death. Diabetes, 51(4):1157-1165.

[18]Szmit, S., Opolski, G., 2006. Diabetic microangiopathy—a current look at the pathogenesis and the clinical implications for cardiovascular diseases. Przegl. Kardiodiab., 1(1):27-34 (in Polish).

[19]Thorand, B., Baumert, J., Chambless, L., et al., 2006. Elevated markers of endothelial dysfunction predict type 2 diabetes mellitus in middle-aged men and women from the general population. Arterioscler. Thromb. Vasc. Biol., 26(2):398-405.

[20]Żukowska-Szczechowska, E., Wystrychowski, G., 2007. Diabetic nephropathy and cardiovascular risk. Przegl. Kardiodiab., 2(4):209-213 (in Polish).