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Plasma Gamma-Glutamyltransferase Is Strongly Determined by Acylation Stimulating Protein Levels Independent of Insulin Resistance in Patients with Acute Coronary Syndrome

机译:血浆γ-谷氨酰转移酶是由酰化刺激蛋白水平强烈决定的独立于急性冠脉综合征患者的胰岛素抵抗

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摘要

Background. Steatosis is a manifestation of the metabolic syndrome often associated with release of liver enzymes and inflammatory adipocytokines linked to cardiovascular risk. Gamma-glutamyltransferase (GGT) is one sensitive liver marker recently identified as an independent cardiovascular risk factor. Mechanisms involved in enhanced hepatic lipogenesis causing steatosis are not yet identified and are usually linked to insulin resistance (IR). Acylation stimulating protein (ASP), a potent lipogenic factor, was recently shown to increase in patients with steatosis and was implicated in its pathogenesis. Aim. To investigate the association of plasma ASP levels with liver and metabolic risk markers in acute coronary syndrome (ACS) patients. Methods. 28 patients and 30 healthy controls were recruited. Their anthropometrics, lipid profile, liver markers, insulin, and ASP levels were measured. Results. In the patients, ASP, liver, and metabolic risk markers were markedly higher than in the controls. ASP strongly predicted GGT levels (B = 0.75, P < 0.0001), followed by triglycerides (B = 0.403, P = 0.017), together determining 57.6% variation in GGT levels. Insulin and IR correlated with metabolic risk components but not with liver enzymes. Conclusion. The strong association of ASP with GGT in ACS patients suggests that ASP, independent of IR, may contribute to a vicious cycle of hepatic lipogenic stimulation and GGT release promoting atherogenesis.
机译:背景。脂肪变性是代谢综合症的一种表现,通常与肝脏酶的释放和与心血管疾病风险相关的炎性脂肪细胞因子有关。 γ-谷氨酰转移酶(GGT)是一种敏感的肝标志物,最近被确定为独立的心血管危险因素。尚无法确定与引起脂肪变性的肝脂肪形成有关的机制,通常与胰岛素抵抗(IR)有关。脂酰化刺激蛋白(ASP)是一种有效的脂肪生成因子,最近在脂肪变性患者中显示增加,并且与其发病机理有关。目标。调查血浆ASP水平与急性冠状动脉综合征(ACS)患者的肝脏和代谢风险标志物的关联。方法。招募了28位患者和30位健康对照。测量了他们的人体测量学,脂质分布,肝标志物,胰岛素和ASP水平。结果。在患者中,ASP,肝脏和代谢风险指标显着高于对照组。 ASP强烈预测了GGT的水平(B = 0.75,P <0.0001),然后是甘油三酸酯(B = 0.403,P = 0.017),共同确定了GGT水平的57.6%变化。胰岛素和IR与代谢风险成分相关,但与肝酶无关。结论。 ACS患者中ASP与GGT的密切联系表明,独立于IR的ASP可能导致肝脏脂肪生成刺激和GGT释放促进动脉粥样硬化的恶性循环。

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