用脂肪來燃燒脂肪,？聽起來像是天方夜譚，然而哈佛醫(yī)學(xué)院的最新研究證明,，一種鮮為人知的脂肪組織——紅脂肪（brown fat）可以燃燒卡路里,，影響機(jī)體的能量代謝系統(tǒng),，有效減輕體重。
在大多數(shù)人看來,，除了能夠保持體溫和貯存能量之外,，脂肪對(duì)人體來說幾乎是有害無益。然而事實(shí)上,，人體內(nèi)存在兩種不同的脂肪：白脂肪與紅脂肪,。白脂肪一直以來便是令節(jié)食者無可奈何的罪魁禍?zhǔn)祝欢t脂肪卻與之截然不同,，它不僅含有大量的線粒體(mitochondria)——一種相當(dāng)于能量生產(chǎn)機(jī)器的人體細(xì)胞,，它能燃燒卡路里以提供熱量。
嬰兒體內(nèi)含有大量的紅脂肪以維持體溫,，然而在成年人體內(nèi),，紅脂肪卻幾乎是無跡可尋。通過基因?qū)嶒?yàn),，科學(xué)家證明,，一些所謂的肌肉前體細(xì)胞（muscle precursor cell）也有可能轉(zhuǎn)變?yōu)榧t脂肪。
哈佛醫(yī)學(xué)院的細(xì)胞生物學(xué)家布魯斯·斯皮格曼（Bruce Spiegelman）的早期研究證明,，加入PRDM16基因可使白脂肪轉(zhuǎn)化為紅脂肪,。在被抽取的脂肪或肌肉前體細(xì)胞內(nèi)植入觸發(fā)型基因（genetic trigger）便可在人體內(nèi)形成紅脂肪供應(yīng)系統(tǒng)，迅速燃燒多余的脂肪,。
作為《自然》雜志上紅脂肪論文的合著者之一的斯皮格曼認(rèn)為,，理論上，這項(xiàng)技術(shù)可以影響整個(gè)機(jī)體的能量代謝系統(tǒng),。對(duì)于這項(xiàng)技術(shù)是否會(huì)阻礙肌肉形成的疑問,，他表示，肌肉前體細(xì)胞可以自我增殖,。當(dāng)少量細(xì)胞變異為紅脂肪后,，留下的空位很快便會(huì)為新生細(xì)胞所填補(bǔ)。
哈佛大學(xué)醫(yī)學(xué)院的曾玉華（Yu-Hua Tseng）和羅納德·卡恩（C. Ronald Kahn）領(lǐng)導(dǎo)下的另一研究小組則發(fā)現(xiàn)了影響紅細(xì)胞形成的另一關(guān)鍵因素—— BMP7基因,。當(dāng)老鼠體內(nèi)的BMP7過量時(shí),，將會(huì)產(chǎn)生大量紅細(xì)胞，而白細(xì)胞卻幾乎停止了增長(zhǎng),。因此,，紅細(xì)胞增加，隨著由此導(dǎo)致的機(jī)體耗能的增加,，實(shí)驗(yàn)老鼠的體重也明顯減輕,。
目前這些發(fā)現(xiàn)僅局限于實(shí)驗(yàn)室里的小白鼠，一旦證實(shí)它們同樣適用于人類，這項(xiàng)技術(shù)將為人們保持體型提供新的捷徑,，減肥人士亦無須再忍受節(jié)食之苦,。斯德哥爾摩大學(xué)（University of Stockholm）的脂肪細(xì)胞專家芭芭拉·坎農(nóng)（Barbara Cannon）分析指出，這些研究成果使人們向最終目標(biāo)邁出了關(guān)鍵的一步——使紅脂肪族成為抵御肥胖癥的有效手段,。
不過,，曾玉華強(qiáng)調(diào)說，目前對(duì)于一般人而言,，節(jié)食和運(yùn)動(dòng)仍是減肥的最佳手段,。然而對(duì)于那些遺傳性肥胖癥患者來說，注射BMP7為他們恢復(fù)健康體型帶來了新的希望,。作為基因觸發(fā)藥物的開發(fā)者之一,，斯皮格曼亦建議人們謹(jǐn)慎行事。他表示,，目前仍不能確定發(fā)揮減肥功效所需的紅脂肪具體數(shù)量是多少,。對(duì)于人類而言，這項(xiàng)技術(shù)尚未完全成熟,，然而不管怎樣,，這是一個(gè)振奮人心的好消息。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 454, 1000-1004 (21 August 2008) | doi:10.1038/nature07221
New role of bone morphogenetic protein 7 in brown adipogenesis and energy expenditure
Yu-Hua Tseng1, Efi Kokkotou3, Tim J. Schulz1, Tian Lian Huang1, Jonathon N. Winnay1, Cullen M. Taniguchi1, Thien T. Tran1, Ryo Suzuki1, Daniel O. Espinoza1, Yuji Yamamoto1, Molly J. Ahrens4, Andrew T. Dudley4, Andrew W. Norris5, Rohit N. Kulkarni2 & C. Ronald Kahn1
Adipose tissue is central to the regulation of energy balance. Two functionally different types of fat are present in mammals: white adipose tissue, the primary site of triglyceride storage, and brown adipose tissue, which is specialized in energy expenditure and can counteract obesity1. Factors that specify the developmental fate and function of white and brown adipose tissue remain poorly understood2, 3. Here we demonstrate that whereas some members of the family of bone morphogenetic proteins (BMPs) support white adipocyte differentiation, BMP7 singularly promotes differentiation of brown preadipocytes even in the absence of the normally required hormonal induction cocktail. BMP7 activates a full program of brown adipogenesis including induction of early regulators of brown fat fate PRDM16 (PR-domain-containing 16; ref. 4) and PGC-1 (peroxisome proliferator-activated receptor- (PPAR) coactivator-1; ref. 5), increased expression of the brown-fat-defining marker uncoupling protein 1 (UCP1) and adipogenic transcription factors PPAR and CCAAT/enhancer-binding proteins (C/EBPs), and induction of mitochondrial biogenesis via p38 mitogen-activated protein (MAP) kinase-(also known as Mapk14) and PGC-1-dependent pathways. Moreover, BMP7 triggers commitment of mesenchymal progenitor cells to a brown adipocyte lineage, and implantation of these cells into nude mice results in development of adipose tissue containing mostly brown adipocytes. Bmp7 knockout embryos show a marked paucity of brown fat and an almost complete absence of UCP1. Adenoviral-mediated expression of BMP7 in mice results in a significant increase in brown, but not white, fat mass and leads to an increase in energy expenditure and a reduction in weight gain. These data reveal an important role of BMP7 in promoting brown adipocyte differentiation and thermogenesis in vivo and in vitro, and provide a potential new therapeutic approach for the treatment of obesity.
