瑞典研究人員最近在研究某些糖尿病患者體內(nèi)胰島素分泌失常原因過程中發(fā)現(xiàn),，一種關(guān)鍵細(xì)胞中的基因變異導(dǎo)致了胰島素分泌失常,，這一發(fā)現(xiàn)有望為糖尿病治療開辟新路。
胰島素是促進(jìn)合成代謝的激素,，也是保證人體內(nèi)血糖處于正常水平的主要激素之一,。一些人之所以患上糖尿病，就是因?yàn)轶w內(nèi)負(fù)責(zé)分泌胰島素的胰島β細(xì)胞不能正常發(fā)揮作用,。
據(jù)此間媒體報(bào)道,，卡羅林斯卡醫(yī)學(xué)院研究人員發(fā)現(xiàn)，人體內(nèi)一旦需要胰島素供應(yīng),，一種名為ＩｎｓＰ７的特殊分子便會(huì)發(fā)出增加胰島素分泌的信號(hào),，而ＩＩ型糖尿病患者的胰腺β細(xì)胞中,，負(fù)責(zé)調(diào)控這種特殊分子的基因發(fā)生了變異，從而導(dǎo)致胰腺β細(xì)胞不能正常分泌人體所需的胰島素,。
研究項(xiàng)目的負(fù)責(zé)人奧洛夫·貝里格倫教授說,，這一發(fā)現(xiàn)具有重要意義，它給糖尿病治療帶來新思路,。人們今后可以開發(fā)能修復(fù)控制ＩｎｓＰ７的基因的方法，從而促使胰腺β細(xì)胞正常分泌胰島素,。
有關(guān)研究成果發(fā)表在最新一期美國《科學(xué)》雜志上,。（新華網(wǎng)）
原始出處:
Science 23 November 2007:
Vol. 318. no. 5854, pp. 1299 - 1302
DOI: 10.1126/science.1146824
Requirement of Inositol Pyrophosphates for Full Exocytotic Capacity in Pancreatic β Cells
Christopher Illies,1 Jesper Gromada,2 Roberta Fiume,1 Barbara Leibiger,1 Jia Yu,1 Kirstine Juhl,3 Shao-Nian Yang,1 Deb K. Barma,4 John R. Falck,4 Adolfo Saiardi,5 Christopher J. Barker,1* Per-Olof Berggren1
Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic β cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in β cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic β cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.
1 The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.
2 Diabetes and Metabolism Disease Area, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
3 Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
4 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
5 U.K. Medical Research Council (MRC) Cell Biology Unit and Laboratory for Molecular Cell Biology, Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK.
* To whom correspondence should be addressed. E-mail: [email protected]
