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   方舟子昨天整理了他对蒙牛牛奶事件的各种看法，弄了个全本，题为《我与蒙牛特仑苏牛奶的战争》,其中一段说：蒙牛公司近日向媒体出示了一张“新西兰农业及林业局食品安全认证”，这是新西兰TATUA公司于2007年2月将原料出口到中国时出具的，但是在这份文件中，该公司出口到中国的原料写的并非MBP，而是“Lactoferrin Co-Isolate”（乳铁蛋白共分离物）。这个原料都有什么成分呢？据新西兰TATUA公司网站的介绍，乳铁蛋白共分离物的成分包括“乳铁蛋白、乳过氧化物酶、生长因子、免疫球蛋白和溶菌酶。”这些成分中，乳铁蛋白、乳过氧化物酶、免疫球蛋白和溶菌酶都与造骨无关，公认与造骨可能有关的只有生长因子，包括IGF-1。日本雪印牛奶公司在试图解释为何牛奶碱性蛋白MBP能促进骨代谢时，列举的理由之一也是因为MBP含有多种生长因子，并举了一篇论文为证，该论文指出，牛奶乳清蛋白的碱性馏分之所以能刺激细胞生长，与乳铁蛋白、乳过氧化物酶、免疫蛋白等无关，而是因为含有包括IGF-1在内的生长因子。所以绕了这么大一圈子，蒙牛的“造骨牛奶蛋白”OMP还是没法摆脱和IGF-1的关系(XYS20090219)。

   最重要的一句是：“这些成分中，乳铁蛋白、乳过氧化物酶、免疫球蛋白和溶菌酶都与造骨无关，公认与造骨可能有关的只有生长因子，包括IGF-1”。

   事实是怎么回事呢？其实，乳铁蛋白lactoferrin就是公认的促进造骨生理过程的物质。2005年5月，新西兰奥克兰大学（University of Auckland）医学系的Dorit Naot博士等人在国际主流专业杂志《临床医学与研究》上发表一篇研究报告，标题就是《乳铁蛋白--一种新发现的骨成长因子》（Lactoferrin – A Novel Bone Growth Factor）。该文说，我们最近揭示了乳铁蛋白在促进骨成长中的作用。在生理浓度范围内，乳铁蛋白强有力地刺激和促进造骨细胞的增殖和分化。在体外培养条件下，乳铁蛋白抑制破骨细胞的发生，在体内研究中，也发现乳铁蛋白促进骨生长的作用（摘要附后）。

   可见，方舟子的“这些成分中，乳铁蛋白、乳过氧化物酶、免疫球蛋白和溶菌酶都与造骨无关，公认与造骨可能有关的只有生长因子，包括IGF-1”，是胡说八道。

   方舟子是蒙牛特仑苏牛奶致癌谣言的始作俑者，尽管他承认“事实上我一开始就不太相信蒙牛真的像其专利声称的那样加了那么多的IGF-1，因为IGF-1是很昂贵的”，但是，他丝毫不打算澄清特仑苏牛奶致癌的谣言，却仅仅咬住“蒙牛此前一直在做虚假宣传”。蒙牛作了虚假宣传，方舟子就提出要重罚蒙牛上百亿元，要蒙牛倒掉而后快。但是，方舟子借蒙牛的虚假宣传，明知故犯地造谣说蒙牛特仑苏牛奶致癌，却一脸理直气壮、大义凛然的样子。为了打假，就可以造假来打假吗？为什么这种明目张胆的造假欺骗行为，就可以被忽略、被容许？

   Lactoferrin – A Novel Bone Growth Factor

   Dorit Naot, PhD; Andrew Grey, MD; Ian R. Reid, MD; Jillian Cornish, PhD; Department of Medicine, University of Auckland, Private Bag 92019, Auckland, New Zealand.

   Lactoferrin is an iron-binding glycoprotein that belongs to the transferrin family. It is present in breast milk, in epithelial secretions, and in the secondary granules of neutrophils. In healthy subjects lactoferrin circulates at concentrations of 2–7 x 10−6 g/ml. Lactoferrin is a pleiotropic factor with potent antimicrobial and immunomodulatory activities. Recently, we have shown that lactoferrin can also promote bone growth. At physiological concentrations, lactoferrin potently stimulates the proliferation and differentiation of primary osteoblasts and also acts as a survival factor inhibiting apoptosis induced by serum withdrawal. Lactoferrin also affects osteoclast formation and, in murine bone marrow culture, lactoferrin potently inhibits osteoclastogenesis. In vivo, local injection of lactoferrin above the hemicalvaria of adult mice results in substantial increases in the dynamic histomorphometric indices of bone formation and bone area.

   The mitogenic effect of lactoferrin in osteoblast-like cells is mediated mainly through LRP1, a member of the family of low-density lipoprotein receptor-related proteins that are primarily known as endocytic receptors. Using confocal laser scanning microscopy, we demonstrated that fluorescently labeled lactoferrin is endocytosed and can be visualized in the cytoplasm of primary osteoblastic cells. Lactoferrin also induces activation of p42/44 MAPK signaling in primary osteoblasts, but the two pathways seem to operate independently as activation of MAPK signaling, but not endocytosis, is necessary for the mitogenic effect of lactoferrin. We conclude that lactoferrin may have a physiological role in bone growth and healing, and a potential therapeutic role as an anabolic factor in osteoporosis.

   http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1183439