德國(guó)馬克斯·普朗克生物物理化學(xué)研究所研究人員通過(guò)激活患糖尿病老鼠胰腺細(xì)胞的一種基因,，使一些胰腺細(xì)胞轉(zhuǎn)化為能分泌胰島素的細(xì)胞,。這一成果為糖尿病治療研究帶來(lái)了新思路。
胰島β細(xì)胞具有分泌胰島素并以此降血糖的功能,，而胰高血糖素的作用與胰島素相反，能使血糖升高,，兩者共同作用可以調(diào)節(jié)機(jī)體血糖平衡,。德國(guó)研究人員發(fā)現(xiàn)，通過(guò)激活患糖尿病老鼠的胰腺細(xì)胞Pax4基因,，不僅可以使胰腺分泌的前體細(xì)胞轉(zhuǎn)化為能分泌胰島素的胰島β細(xì)胞,，而且還能使原來(lái)分泌胰高血糖素的細(xì)胞轉(zhuǎn)化為胰島β細(xì)胞。
參與這項(xiàng)研究的專家說(shuō),，在老鼠身上發(fā)現(xiàn)的上述基因調(diào)節(jié)機(jī)制能否用于人還需更多研究加以證實(shí),。如果將來(lái)可以依據(jù)上述發(fā)現(xiàn)研發(fā)糖尿病藥物，還需要考慮各種因素，例如不能導(dǎo)致胰島β細(xì)胞過(guò)多生成,，否則會(huì)破壞胰島素和胰高血糖素之間的微妙平衡,。
這一研究成果已發(fā)表在新一期美國(guó)學(xué)術(shù)期刊《細(xì)胞》（Cell）上。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell, Volume 138, Issue 3, 449-462, 7 August 2009 doi:10.1016/j.cell.2009.05.035
The Ectopic Expression of Pax4 in the Mouse Pancreas Converts Progenitor Cells into and Subsequently Cells
Patrick Collombat1,2,3,11,,,Xiaobo Xu4,Philippe Ravassard3,5,Beatriz Sosa-Pineda6,Sébastien Dussaud5,7,Nils Billestrup8,Ole D. Madsen2,3,9,Palle Serup2,3,9,Harry Heimberg2,3,4andAhmed Mansouri1,2,10,,
1 Department of Molecular Cell Biology, Max-Planck Institute for Biophysical Chemistry, Am Fassberg, D-37077 G?ttingen, Germany
2 Beta Cell Biology Consortium, 2213 Garland Avenue, 9465 MRB IV, Nashville, TN 37323-0494, USA
3 JDRF Center for Beta Cell Therapy in Diabetes, Laarbeeklaan 103, B-1090 Brussels, Belgium
4 Diabetes Research Center, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium
5 Biotechnology and Biotherapy Laboratory, Centre de Recherche de l'Institut du Cerveau et de la Moelle, CNRS UMR 7225, INSERM UMRS 975, University Pierre et Marie Curie, H?pital Pitié Salpêtrière, FR-75013 Paris, France
6 Department of Genetics/Tumor Cell Biology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105-3678, USA
7 Centre d'Expérimentation Fonctionnelle, Pitié Salpêtrière Medical Faculty, Université Pierre et Marie Curie, FR-75013 Paris, France
8 Department of Translational Diabetology Research Institute, Hagedorn Niels Steensensvej 6, DK-2820 Gentofte, Denmark
9 Department of Developmental Biology Research Institute, Hagedorn Niels Steensensvej 6, DK-2820 Gentofte, Denmark
10 Department of Clinical Neurophysiology, University of Göttingen, Robert-Koch Strasse 40, D-37075 G?ttingen, Germany
We have previously reported that the loss of Arx and/or Pax4 gene activity leads to a shift in the fate of the different endocrine cell subtypes in the mouse pancreas, without affecting the total endocrine cell numbers. Here, we conditionally and ectopically express Pax4 using different cell-specific promoters and demonstrate that Pax4 forces endocrine precursor cells, as well as mature α cells, to adopt a β cell destiny. This results in a glucagon deficiency that provokes a compensatory and continuous glucagon+ cell neogenesis requiring the re-expression of the proendocrine gene Ngn3. However, the newly formed β cells fail to correct the hypoglucagonemia since they subsequently acquire a β cell phenotype upon Pax4 ectopic expression. Notably, this cycle of neogenesis and redifferentiation caused by ectopic expression of Pax4 in β cells is capable of restoring a functional β cell mass and curing diabetes in animals that have been chemically depleted of β cells.
