von Eynatten Maximilian, Schneider Jochen G, Humpert Per M, Rudofsky Gottfried, Schmidt Nikolaus, Barosch Patrizia, Hamann Andreas, Morcos Michael, Kreuzer Joerg, Bierhaus Angelika, Nawroth Peter P, Dugi Klaus A
Department of Medicine I (Endocrinology and Metabolism), University of Heidelberg, INF 410, D-69120 Heidelberg, Germany.
Diabetes Care. 2004 Dec;27(12):2925-9. doi: 10.2337/diacare.27.12.2925.
Adiponectin is a plasma protein expressed in adipose tissue. Hypoadiponectinemia is associated with low HDL cholesterol and high plasma triglycerides, which also characterize lipoprotein lipase (LPL) deficiency syndromes. Recently, dramatically increased LPL activity was reported in mice overexpressing adiponectin. We therefore speculated that adiponectin may directly affect LPL in humans.
We measured plasma adiponectin and postheparin LPL in 206 nondiabetic men and in a second group of 110 patients with type 2 diabetes. Parameters were correlated with markers of systemic inflammation (C-reactive protein [CRP]) and insulin resistance (homeostatis model assessment of insulin resistance [HOMA-IR]).
Nondiabetic subjects with decreased plasma adiponectin had lower LPL activity (r=0.42, P <0.0001). This association of plasma adiponectin with LPL activity was confirmed in the second group of patients with type 2 diabetes (r=0.37, P <0.0001). Multivariate analysis revealed that adiponectin was the strongest factor influencing LPL activity, accounting for 23% of the variation in LPL activity in nondiabetic subjects and for 26% of the variation in LPL activity in type 2 diabetic patients. These associations were independent of plasma CRP and HOMA-IR.
These results demonstrate an association of decreased postheparin LPL activity with low plasma adiponectin that is independent of systemic inflammation and insulin resistance. Therefore, LPL may represent a link between low adiponectin levels and dyslipidemia in both nondiabetic individuals and patients with type 2 diabetes.
脂联素是一种在脂肪组织中表达的血浆蛋白。低脂联素血症与低高密度脂蛋白胆固醇和高血浆甘油三酯有关，这也是脂蛋白脂肪酶（LPL）缺乏综合征的特征。最近，有报道称在过度表达脂联素的小鼠中LPL活性显著增加。因此，我们推测脂联素可能直接影响人类的LPL。
我们测量了206名非糖尿病男性以及另一组110名2型糖尿病患者的血浆脂联素和肝素后LPL。各项参数与全身炎症标志物（C反应蛋白[CRP]）和胰岛素抵抗（胰岛素抵抗稳态模型评估[HOMA-IR]）相关。
血浆脂联素降低的非糖尿病受试者LPL活性较低（r = 0.42，P <0.0001）。在第二组2型糖尿病患者中也证实了血浆脂联素与LPL活性的这种关联（r = 0.37，P <0.0001）。多变量分析显示，脂联素是影响LPL活性的最强因素，在非糖尿病受试者中占LPL活性变异的23%，在2型糖尿病患者中占LPL活性变异的26%。这些关联独立于血浆CRP和HOMA-IR。
这些结果表明肝素后LPL活性降低与低血浆脂联素有关，且独立于全身炎症和胰岛素抵抗。因此，LPL可能是连接非糖尿病个体和2型糖尿病患者低脂联素水平与血脂异常的一个环节。
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