今年早些时候，美国等国研究人员相继发现，不仅新生儿体内有可燃烧脂肪并产生热量的棕色脂肪细胞，成人体内也有这种细胞，只不过不太活跃。德国研究人员日前又报告说，他们发现一种蛋白激酶，对棕色脂肪细胞的产生和功能有重要调节作用。通过激活这种蛋白激酶信号通路，或许有助于找到减肥新法。
棕色脂肪细胞和白色脂肪细胞扮演着不同的角色。白色脂肪细胞的主要功能是储存脂肪，而棕色脂肪细胞则将脂肪转化为热量。以往人们认为新生儿有许多棕色脂肪以帮助他们保暖，但棕色脂肪会随着人的成长而迅速消失。今年，研究人员发现成人颈部也有棕色脂肪细胞储存，但体重过重的人这些棕色脂肪细胞很不活跃，甚至完全缺失。
德国波恩大学日前发表公报说，该大学和德国其他一些研究机构合作研究发现，由蛋白激酶G（PKG）调控的一个信号通路可调节脂肪组织干细胞分化为棕色脂肪细胞。此外，蛋白激酶G还可使棕色脂肪细胞对胰岛素敏感，由此蛋白激酶G可对燃烧的脂肪量起调节作用。
研究人员估计，成人棕色脂肪组织失调会导致体重过重。如果人体这种“天然加热器”能被重新激活，则可以找到一种理想的“以肥治肥”的减肥法。按研究人员估算，50克活跃的棕色脂肪组织就可以将人体静态能量消耗值提高20％。（生物谷Bioon.com）
棕色脂肪相关研究：
Nature：一种双单元分子开关可控棕色脂肪细胞生成
Cell Metabolism：再生棕色脂肪细胞可治疗肥胖
Nature：脂肪与肌肉之间的联系
Cell Metabolism：脂肪代谢研究
Nature ：BMP-7与肥胖症的关系
Science：2008年十大科学进展——另一种颜色的脂肪
生物谷推荐原始出处：
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.
