据6月18日的《科学》杂志报道说，科学家们已经发现了一种由脂肪细胞产生的蛋白质，这种蛋白质就像是这些细胞所产生的其它蛋白一样，它实际上对代谢健康会有良好功效。 如果研究人员能够找到一种用新的药物来来控制它的方法，这种叫做Sfrp5的蛋白可能是抵抗如在肥胖者中的II型糖尿病这样的代谢性疾病的有利武器。 大多数的由脂肪细胞分泌的“脂肪细胞因子”可增强炎症和胰岛素的抵抗力。 这就是为什么肥胖者容易产生II型糖尿病和其它代谢性疾病的主要原因之一。 为了寻找新的脂肪因子，Noriyuki Ouchi及其同僚对来自精瘦小鼠和肥胖小鼠脂肪组织的基因表达特征做了比较。 他们发现，Sfrp5在来自肥胖小鼠的脂肪组织以及在胖人腹部脂肪的活检组织中要更为丰富。 在肥胖的小鼠中，Sfrp5可抑制关键性的炎症细胞（称作巨噬细胞，它们处于脂肪组织之中）的激活，而其之所以能够做到这一点看来是通过抑制JNK信号转导通路。 对Sfrp5和JNK信号转导分子之间相互作用的更多的研究也许能够开启研发治疗与肥胖症有关的代谢性疾病药物的新机会。
Article #29: "Sfrp5 Is an Anti-Inflammatory Adipokine That Modulates Metabolic Dysfunction in Obesity," by N. Ouchi; A. Higuchi; K. Ohashi; Y. Oshima; N. Gokce; Y. Akasaki; K. Walsh at Boston University School of Medicine in Boston, MA; R. Shibata at Nagoya University Graduate School of Medicine in Nagoya, Japan; A. Shimono at National University of Singapore in Singapore, Singapore.
Sfrp5 Is an Anti-Inflammatory Adipokine That Modulates Metabolic Dysfunction in Obesity
Published Online June 17, 2010
Science DOI: 10.1126/science.1188280
Adipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a protein previously linked to the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression is perturbed in models of obesity and type 2 diabetes. Sfrp5-deficient mice on a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages that was associated with activation of the JNK signaling pathway. Adenovirus-mediated delivery of Sfrp5 to mouse models of obesity ameliorated glucose intolerance and hepatic steatosis. Thus, in the setting of obesity, Sfrp5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue.
