发表在2014年1月的FASEB Journal杂志上的一项最新研究中，科学家证实随着年龄的增长，棕色脂肪的产热活动减少。

　　棕色脂肪是“好”脂肪，坐落在我们的脖子的背部，帮助燃烧“坏的”白色脂肪。此外，研究人员还发现了一个可能的代谢开关，可以重新激活棕色脂肪。

　　Junko Sugatanii博士表示：研究是关于PAF / PAFR如何通过调控动物以及人类的棕色脂肪中β3 -AR生成信号控制UCP1的水平，研究可发现新的治疗靶点来治疗与肥胖症相关的代谢紊乱。

　　为了获得这一发现，科学家分析了两组小鼠。第一组血小板活化因子受体（PAFR）基因敲除小鼠。第二组是正常小鼠。与野生型同窝小鼠相比，PAFR缺陷的小鼠随着年龄增长发展了更严重的肥胖状态，具有更高的身体和附睾脂肪量。

　　从PAFR基因敲除小鼠模型结果显示，PAFR缺乏会导致褐色脂肪组织（BAT）功能障碍，从而诱发肥胖的发展，由于BAT产热作用受损。该研究阐明了PAF/PAF受体介导抗肥胖相关的分子机制，将有助发现肥胖症和相关病症如糖尿病，高血压，心脏疾病，癌症，不育和溃疡等治疗的新靶标。

　　原文阅读：

　　Abstract

　　Platelet-activating factor receptor (PAFR)-deficient mice developed a more severe obese state characterized by higher body mass (?25%) and epididymal fat mass (?55%) with age than that of wild-type (WT) littermates. PAFR-deficient mice did not show changes in the expression of critical genes involved in anabolic and catabolic metabolism in adipose, liver, and muscle tissues between 6 and 36 wk. However, a 38?81% reduction in β3/β1-adrenergic receptor (AR) and uncoupling protein 1 (UCP1) mRNA and protein levels was observed in the interscapular brown adipose tissue (BAT) of PAFR-deficient mice. Whereas a single injection of the β3-adrenergic agonist, CL-316,243 (25 μg/kg) increased temperatures in the brown fat and rectums of WT mice, this increase in temperature was markedly suppressed in PAFR-deficient mice. Acetyl-CoA:lyso-platelet-activating factor (PAF) acetyltransferase, which is involved in PAF biosynthesis, and the PAF receptor were predominantly localized in BAT macrophages, whereas brown adipocytes possessed the enzyme and functional PAF receptors. The stimulation of brown adipocytes by PAF induced the expression of β3-AR mRNA and protein (1.5- and 1.9-fold, respectively), but not that of UCP1. These results indicate that obesity in PAFR-deficient mice resulted from impaired BAT activity and suggest that the antiobese function of PAF occurs through β3-AR/UCP1 expression in BAT.