本期封面所示為棕色脂肪,，在其中，PRDM16的表達(dá)被shRNA抑制,，肌肉細(xì)胞標(biāo)記為紅色,，脂肪細(xì)胞和其他細(xì)胞類型標(biāo)記為藍(lán)色核。封面美術(shù)：Eric Smith,。
人體中有兩種類型的脂肪組織：一種是棕色脂肪,，主要功能是燃燒卡路里，產(chǎn)生身體所需熱量,；另一種是白色脂肪,，用來儲(chǔ)存能量。
現(xiàn)在,，研究人員獲得一個(gè)令人吃驚的發(fā)現(xiàn)：棕色脂肪是骨骼肌的一種衍生物,。這一發(fā)現(xiàn)也許會(huì)促使我們?nèi)ブ匦滤伎嘉覀冴P(guān)于這兩種組織之間關(guān)系的觀點(diǎn)。以前,，關(guān)于脂肪發(fā)育的大多數(shù)模型都認(rèn)為,，棕色和白色脂肪細(xì)胞來自同一種成脂肪前體細(xì)胞，但體內(nèi)細(xì)胞系跟蹤研究表明,，棕色脂肪細(xì)胞起源于表達(dá)Myf5基因（迄今只在肌肉細(xì)胞中發(fā)現(xiàn)的一種標(biāo)記）的成骨細(xì)胞,。PRDM16（一種鋅指蛋白，已知能夠刺激棕色脂肪選擇性基因表達(dá)）可強(qiáng)有力地調(diào)控肌肉與棕色脂肪之間的雙向細(xì)胞命運(yùn)轉(zhuǎn)換,。作為棕色脂肪細(xì)胞命運(yùn)的一種支配性調(diào)控因子,，PRDM16在治療肥胖癥上可能有潛在用途，能夠誘導(dǎo)PRDM16在白色脂肪或肌肉前體中表達(dá)的化合物也可能有這種作用,。(生物谷Bioon.com）
生物谷推薦原始出處：
Nature 454, 961-967 (21 August 2008) | doi:10.1038/nature07182
PRDM16 controls a brown fat/skeletal muscle switch
Patrick Seale1, Bryan Bjork2, Wenli Yang1, Shingo Kajimura1, Sherry Chin1, Shihuan Kuang3, Anthony Scimè3, Srikripa Devarakonda1, Heather M. Conroe1, Hediye Erdjument-Bromage4, Paul Tempst4, Michael A. Rudnicki3, David R. Beier2 & Bruce M. Spiegelman1
Dana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, 1 Jimmy Fund Way, Boston, Massachusetts 02115, USA
Genetics Division, Brigham and Women's Hospital, Harvard Medical School, New Research Building, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
The Sprott Center for Stem Cell Research, Ottawa Health Research Institute, Molecular Medicine Program, 501 Smyth Road, Ottawa, Ontario K1H 8L6, Canada
Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA
Brown fat can increase energy expenditure and protect against obesity through a specialized program of uncoupled respiration. Here we show by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5, a gene previously thought to be expressed only in the myogenic lineage. We also demonstrate that the transcriptional regulator PRDM16 (PRD1-BF1-RIZ1 homologous domain containing 16) controls a bidirectional cell fate switch between skeletal myoblasts and brown fat cells. Loss of PRDM16 from brown fat precursors causes a loss of brown fat characteristics and promotes muscle differentiation. Conversely, ectopic expression of PRDM16 in myoblasts induces their differentiation into brown fat cells. PRDM16 stimulates brown adipogenesis by binding to PPAR- (peroxisome-proliferator-activated receptor-) and activating its transcriptional function. Finally, Prdm16-deficient brown fat displays an abnormal morphology, reduced thermogenic gene expression and elevated expression of muscle-specific genes. Taken together, these data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myoblast markers and is not involved in white adipogenesis.
