Konukoglu Dildar, Kemerli Gülhan Demiriz, Sabuncu Tevfik, Hatemi Hüsrev
Department of Biochemistry, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey.
Clin Invest Med. 2003 Dec;26(6):279-84.
Diabetic patients are at high risk of atherosclerotic complications, and factors associated with this include hypercholesterolemia, hemorheologic disturbances in erythrocytes and oxidative stress. We, therefore, carried out a study in type 2 diabetic patients to determine the relationships of erythrocyte Na+-K+ ATPase activity, plasma cholesterol and oxidative stress in this population.
Erythrocyte Na+-K+ ATPase activity and its relationship between plasma cholesterol and thiobarbituric acid reactive substance (TBARS, a marker of oxidative stress) were studied in type 2 diabetic patients with (n = 26) or without angiopathy (n = 30). Na+-K+ ATPase activity was measured by a colorimetric enzymatic method. Plasma TBARS levels were determined spectrophotometrically. Diabetic patients were classified according to plasma cholesterol concentrations as normo- or hypercholesterolemic (plasma total cholesterol > 5.18 mmol/L).
Diabetic patients with or without angiopathy had lower erythrocyte Na+-K+ ATPase activity (p < 0.001 and p < 0.001 respectively) and higher plasma TBARS levels than healthy subjects (n = 20) (p < 0.001 and p < 0.001 respectively). Na+-K+ ATPase activity in the diabetic patients with angiopathy was lower than in the diabetic patients without angiopathy (p < 0.001). In the diabetic patients both with and without angiopathy, hypercholesterolemic patients had lower erythrocyte Na+-K+ ATPase activity and higher plasma TBARS levels than normocholesterolemic patients (p < 0.001, p < 0.001 respectively) There was no difference in the plasma TBARS concentrations between diabetic patients with and without angiopathy. There were negative correlations between erythrocyte Na+-K+ ATPase activity and both plasma cholesterol (r = -0.72) and plasma TBARS (r = -0.46) and a positive correlation between plasma cholesterol and TBARS (r = 0.42).
Elevated plasma cholesterol may be responsible for the inhibition of erythrocyte Na+-K+ ATPase activity. Together with elevated cholesterol, free radical-induced mechanisms may be involved in the inhibition of Na+-K+ ATPase activity.
糖尿病患者发生动脉粥样硬化并发症的风险很高，与之相关的因素包括高胆固醇血症、红细胞血液流变学紊乱和氧化应激。因此，我们对2型糖尿病患者进行了一项研究，以确定该人群中红细胞钠钾ATP酶活性、血浆胆固醇和氧化应激之间的关系。
研究了26例伴有血管病变和30例不伴有血管病变的2型糖尿病患者红细胞钠钾ATP酶活性及其与血浆胆固醇和硫代巴比妥酸反应物质（TBARS，氧化应激标志物）之间的关系。钠钾ATP酶活性采用比色酶法测定。血浆TBARS水平采用分光光度法测定。糖尿病患者根据血浆胆固醇浓度分为正常胆固醇血症或高胆固醇血症（血浆总胆固醇>5.18 mmol/L）。
伴有或不伴有血管病变的糖尿病患者红细胞钠钾ATP酶活性均低于健康受试者（分别为n = 20）（p < 0.001和p < 0.001），血浆TBARS水平高于健康受试者（分别为p < 0.001和p < 0.001）。伴有血管病变的糖尿病患者钠钾ATP酶活性低于不伴有血管病变的糖尿病患者（p < 0.001）。在伴有和不伴有血管病变的糖尿病患者中，高胆固醇血症患者的红细胞钠钾ATP酶活性低于正常胆固醇血症患者，血浆TBARS水平高于正常胆固醇血症患者（分别为p < 0.001，p < 0.001）。伴有和不伴有血管病变的糖尿病患者血浆TBARS浓度无差异。红细胞钠钾ATP酶活性与血浆胆固醇（r = -0.72）和血浆TBARS（r = -0.46）均呈负相关，血浆胆固醇与TBARS呈正相关（r = 0.42）。
血浆胆固醇升高可能是红细胞钠钾ATP酶活性受抑制的原因。除胆固醇升高外，自由基诱导机制可能也参与了钠钾ATP酶活性的抑制。
