今年早些時(shí)候,，美國等國研究人員相繼發(fā)現(xiàn)，不僅新生兒體內(nèi)有可燃燒脂肪并產(chǎn)生熱量的棕色脂肪細(xì)胞,，成人體內(nèi)也有這種細(xì)胞,，只不過不太活躍。德國研究人員日前又報(bào)告說,，他們發(fā)現(xiàn)一種蛋白激酶,，對棕色脂肪細(xì)胞的產(chǎn)生和功能有重要調(diào)節(jié)作用。通過激活這種蛋白激酶信號通路,，或許有助于找到減肥新法,。
棕色脂肪細(xì)胞和白色脂肪細(xì)胞扮演著不同的角色。白色脂肪細(xì)胞的主要功能是儲存脂肪,，而棕色脂肪細(xì)胞則將脂肪轉(zhuǎn)化為熱量,。以往人們認(rèn)為新生兒有許多棕色脂肪以幫助他們保暖，但棕色脂肪會隨著人的成長而迅速消失,。今年,，研究人員發(fā)現(xiàn)成人頸部也有棕色脂肪細(xì)胞儲存，但體重過重的人這些棕色脂肪細(xì)胞很不活躍,，甚至完全缺失,。
德國波恩大學(xué)日前發(fā)表公報(bào)說，該大學(xué)和德國其他一些研究機(jī)構(gòu)合作研究發(fā)現(xiàn),，由蛋白激酶G（PKG）調(diào)控的一個(gè)信號通路可調(diào)節(jié)脂肪組織干細(xì)胞分化為棕色脂肪細(xì)胞,。此外，蛋白激酶G還可使棕色脂肪細(xì)胞對胰島素敏感,，由此蛋白激酶G可對燃燒的脂肪量起調(diào)節(jié)作用,。
研究人員估計(jì)，成人棕色脂肪組織失調(diào)會導(dǎo)致體重過重,。如果人體這種“天然加熱器”能被重新激活,，則可以找到一種理想的“以肥治肥”的減肥法,。按研究人員估算，50克活躍的棕色脂肪組織就可以將人體靜態(tài)能量消耗值提高20％,。（生物谷Bioon.com）
棕色脂肪相關(guān)研究：
Nature：一種雙單元分子開關(guān)可控棕色脂肪細(xì)胞生成
Cell Metabolism：再生棕色脂肪細(xì)胞可治療肥胖
Nature：脂肪與肌肉之間的聯(lián)系
Cell Metabolism：脂肪代謝研究
Nature ：BMP-7與肥胖癥的關(guān)系
Science：2008年十大科學(xué)進(jìn)展——另一種顏色的脂肪
生物谷推薦原始出處：
Sci. Signal., 1 December 2009 DOI: 10.1126/scisignal.2000511
Protein Kinase G Controls Brown Fat Cell Differentiation and Mitochondrial Biogenesis
Bodo Haas1, Peter Mayer2*, Katja Jennissen1*, Daniela Scholz1, Mauricio Berriel Diaz3, Wilhelm Bloch4, Stephan Herzig3, Reinhard F?ssler5, and Alexander Pfeifer1,6
1 Institute for Pharmacology and Toxicology, Biomedical Center, University of Bonn, 53105 Bonn, Germany.
2 Federal Institute for Drugs and Medical Devices, 53175 Bonn, Germany.
3 Molecular Metabolic Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.
4 Department of Molecular and Cellular Sport Medicine, German Sport University, 50933 Cologne, Germany.
5 Department of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
6 Pharma-Center, University of Bonn, 53105 Bonn, Germany.
Abstract: Brown adipose tissue (BAT) is a primary site of energy expenditure through thermogenesis, which is mediated by the uncoupling protein–1 (UCP-1) in mitochondria. Here, we show that protein kinase G (PKG) is essential for brown fat cell differentiation. Induction of adipogenic markers and fat storage was impaired in the absence of PKGI. Furthermore, PKGI mediated the ability of nitric oxide (NO) and guanosine 3',5'-monophosphate (cGMP) to induce mitochondrial biogenesis and increase the abundance of UCP-1. Mechanistically, we found that PKGI controlled insulin signaling in BAT by inhibiting the activity of RhoA and Rho-associated kinase (ROCK), thereby relieving the inhibitory effects of ROCK on insulin receptor substrate–1 and activating the downstream phosphoinositide 3-kinase–Akt cascade. Thus, PKGI links NO and cGMP signaling with the RhoA-ROCK and the insulin pathways, thereby controlling induction of adipogenic and thermogenic programs during brown fat cell differentiation.
