Kaushik Shalini V, Plaisance Eric P, Kim Teayoun, Huang Edmond Y, Mahurin A Jack, Grandjean Peter W, Mathews Suresh T
Department of Nutrition and Food Science, Auburn University, Auburn, AL 36849, USA.
Diabetes Metab Res Rev. 2009 Jul;25(5):427-34. doi: 10.1002/dmrr.967.
Fetuin-A, a liver-secreted phosphoprotein and physiological inhibitor of insulin receptor tyrosine kinase, is associated with insulin resistance, metabolic syndrome (MetS), and an increased risk for type 2 diabetes. However, studies on the modulation of circulating levels of fetuin-A are limited. The goal of this study was to determine the effect of niacin administration on serum total- and phosphorylated fetuin-A (phosphofetuin-A) concentrations in individuals with MetS and correlate with changes in serum lipids, insulin sensitivity, and markers of inflammation.
Fifteen sedentary, obese, male participants, who met the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria for MetS, were treated with extended-release niacin (Niaspan) for 6 weeks. Blood samples were obtained before and after treatment with niacin.
Serum fetuin-A and phosphofetuin-A concentrations were decreased following niacin administration (p < 0.005). Changes in fetuin-A concentrations were correlated with changes in triglyceride (r = 0.62, p = 0.01) and C-reactive protein (CRP) concentrations (r = 0.58, p < 0.05) after niacin treatment. Changes in high-density lipoproteins (HDL)-cholesterol following niacin intervention were negatively correlated with changes in serum fetuin-A (p < 0.05) and phosphofetuin-A concentrations (p < 0.05). Serum cortisol levels were significantly elevated after niacin administration.
Niacin treatment lowers serum total- and phosphofetuin-A concentrations in individuals with MetS, and these changes correlate with the beneficial changes in serum lipids. Because niacin is known to induce insulin resistance, these findings suggest that fetuin-A may not be a mediator of niacin-induced insulin resistance but it may blunt the insulin resistance induced by niacin by decreasing its circulating concentrations.
胎球蛋白-A是一种肝脏分泌的磷蛋白，也是胰岛素受体酪氨酸激酶的生理抑制剂，与胰岛素抵抗、代谢综合征（MetS）以及2型糖尿病风险增加有关。然而，关于调节循环中胎球蛋白-A水平的研究有限。本研究的目的是确定烟酸给药对患有MetS个体血清总胎球蛋白-A和磷酸化胎球蛋白-A（磷酸胎球蛋白-A）浓度的影响，并与血清脂质、胰岛素敏感性和炎症标志物的变化相关联。
15名符合美国国家胆固醇教育计划成人治疗小组第三次报告（NCEP ATP III）MetS标准的久坐、肥胖男性参与者接受缓释烟酸（Niaspan）治疗6周。在烟酸治疗前后采集血样。
烟酸给药后血清胎球蛋白-A和磷酸胎球蛋白-A浓度降低（p < 0.005）。烟酸治疗后，胎球蛋白-A浓度的变化与甘油三酯（r = 0.62，p = 0.01）和C反应蛋白（CRP）浓度的变化相关（r = 0.58，p < 0.05）。烟酸干预后高密度脂蛋白（HDL）胆固醇的变化与血清胎球蛋白-A（p < 0.05）和磷酸胎球蛋白-A浓度的变化呈负相关（p < 0.05）。烟酸给药后血清皮质醇水平显著升高。
烟酸治疗可降低患有MetS个体的血清总胎球蛋白-A和磷酸胎球蛋白-A浓度，且这些变化与血清脂质的有益变化相关。由于已知烟酸会诱导胰岛素抵抗，这些发现表明胎球蛋白-A可能不是烟酸诱导胰岛素抵抗的介质，但它可能通过降低其循环浓度来减轻烟酸诱导的胰岛素抵抗。
