奥地利研究人员最新发现,刺激一种基因能够抑制动物体内白色脂肪的形成。这一研究成果已刊登在最新一期美国《细胞》杂志上。
成年哺乳动物体内有白色脂肪和棕色脂肪。白色脂肪的主要作用是将体内多余能量以脂肪的形式储存起来,形成通常人们所不愿看到的肥胖,而棕色脂肪能将脂肪转化为热量。
奥地利科学院和萨尔茨堡大学的科研人员对大量动物基因开展研究后发现,基因对体内脂肪形成的干预作用不可忽视,其中被这些研究者称为“刺猬”的一种基因能够作用于成年动物的脂肪组织。而此前研究者认为,这种基因只会在胚胎的成长过程中发挥重要作用。
奥地利科研人员与加拿大多伦多大学的专家合作,通过老鼠实验发现,刺激“刺猬”基因可成功抑制白色脂肪生长,在这一过程中,棕色脂肪仍能正常生长。
参与该研究的专家说,未来有望通过增强人体内“刺猬”基因的活力,抑制白色脂肪的形成,从而治疗肥胖症。(生物谷Bioon.com)
生物谷推荐原始出处:
Cell, Volume 140, Issue 1, 148-160, 8 January 2010
Drosophila Genome-wide Obesity Screen Reveals Hedgehog as a Determinant of Brown versus White Adipose Cell Fate
J. Andrew Pospisilik, Daniel Schramek, Harald Schnidar, Shane J.F. Cronin, Nadine T. Nehme, Xiaoyun Zhang, Claude Knauf, Patrice D. Cani, Karin Aumayr, Jelena Todoric, Martina Bayer, Arvand Haschemi, Vijitha Puviindran, Krisztina Tar, Michael Orthofer, G. Gregory Neely, Georg Dietzl, Armen Manoukian, Martin Funovics, Gerhard Prager, Oswald Wagner, Dominique Ferrandon, Fritz Aberger, Chi-chung Hui, Harald Esterbauer, Josef M. Penninger
Over 1 billion people are estimated to be overweight, placing them at risk for diabetes, cardiovascular disease, and cancer. We performed a systems-level genetic dissection of adiposity regulation using genome-wide RNAi screening in adult Drosophila. As a follow-up, the resulting ~500 candidate obesity genes were functionally classified using muscle-, oenocyte-, fat-body-, and neuronal-specific knockdown in vivo and revealed hedgehog signaling as the top-scoring fat-body-specific pathway. To extrapolate these findings into mammals, we generated fat-specific hedgehog-activation mutant mice. Intriguingly, these mice displayed near total loss of white, but not brown, fat compartments. Mechanistically, activation of hedgehog signaling irreversibly blocked differentiation of white adipocytes through direct, coordinate modulation of early adipogenic factors. These findings identify a role for hedgehog signaling in white/brown adipocyte determination and link in vivo RNAi-based scanning of the Drosophila genome to regulation of adipocyte cell fate in mammals.