Response to comment on: Haider DG, Schaller G, Kapiotis S, Maier C, Luger A, Wolzt M (2006) The release of the adipocytokine visfatin is regulated by glucose and insulin. Diabetologia 49:1909–1914
Response to comment on: Haider DG, Schaller G, Kapiotis S, Maier C, Luger A, Wolzt M (2006) The release of the adipocytokine visfatin is regulated by glucose and insulin. Diabetologia 49:1909–1914
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对评论的回应：Haider DG、Schaller G、Kapiotis S、Maier C、Luger A、Wolzt M (2006) 脂肪细胞因子内脂素的释放受葡萄糖和胰岛素调节 49:1909–1914。
作者：
D. Haider;M. Wolzt
致编辑：我们饶有兴趣地阅读了 Pfützner 和 Forst [1] 对我们最近在 Diabetologia [2] 上发表的文章的评论。健康年轻受试者的循环内脂素浓度通常低于糖尿病患者或有风险的老年受试者。由于目前市面上只有一种带有 CE 标志的 ELISA 检测试剂盒（Phoenix Peptides，卡尔斯鲁厄，德国），因此人们预计报告中生成的数据应该具有可比性。然而，作者已经证明内脂素血清/血浆浓度存在相当大的变化。根据我们的经验，循环内脂素的范围从健康儿童的低至 0.4 ng/ml [3] 到 1 型糖尿病患者的 92.3 ng/ml [4]。该范围与其他研究人员在 2 型糖尿病（范围 2-50 ng/ml）[5, 6] 或妊娠糖尿病（范围 5-90 ng/ml）[7, 8] 患者中提供的数据一致。重要的是，健康年轻志愿者的新鲜样本中的血清/血浆内脂素与-30°C 下保存的样本没有差异。因此，当维持冷冻条件时，内脂素的缓慢分解不太可能解释健康受试者组之间的差异。然而，我们同意这样的评论，即循环内脂素的相当大范围是许多研究中的限制因素，应促使研究人员谨慎对待这些结果，特别是在分析横断面研究时。分析方法引入的系统误差仍可能反映急性介入研究中随时间的变化，即全身内脂素浓度增加，即使幅度减弱或增强。最后，手稿中仅给出了葡萄糖输注过程中的内源性胰岛素浓度，以避免重复发表；读者可以参考之前的出版物，其中提供了更详细的胰岛素浓度 [9]。
To the Editor: We read with interest the comments by Pfützner and Forst [1] on our recent article in Diabetologia [2]. Circulating visfatin concentrations in healthy young subjects are generally lower than those in patients with diabetes or elderly subjects at risk. As there is only one CE-marked ELISA test kit commercially available at the moment (Phoenix Peptides, Karlsruhe, Germany), one would anticipate that data generated should be comparable among reports. However, authors have demonstrated considerable variation in visfatin serum/plasma concentrations. In our experience, circulating visfatin ranges from as low as 0.4 ng/ml in healthy children [3] to 92.3 ng/ml [4] in patients with type 1 diabetes. This range is consistent with data presented by other researchers in patients with type 2 diabetes (range 2–50 ng/ml) [5, 6] or gestational diabetes (range 5–90 ng/ml) [7, 8]. Importantly, serum/plasma visfatin was not different in fresh samples from healthy young volunteers compared with specimens stored at −30°C. The slow decomposition of visfatin is therefore unlikely to account for differences between groups of healthy subjects when freezing conditions are maintained. However, we agree with the comment that the considerable range of circulating visfatin is a limiting factor in many studies and should prompt investigators to treat these results with caution, particularly when cross-sectional studies are being analysed. A systematic error introduced by an analytical method may still reflect changes over time in acute interventional studies, i.e. increased systemic visfatin concentrations, even if the amplitude is attenuated or augmented. Finally, only endogenous insulin concentrations during glucose infusion are given in the manuscript to avoid duplicate publication; the reader is referred to a previous publication where more detailed insulin concentrations are presented [9].