<html> <head> <title>Colin G. Nichols, Ph.D.</title> </head> <body bgcolor="#000000"> <h1 align="center"><img src="../images/Fac_Res_Int.gif" width="640" height="150"></h1> <table width="771" border="0" align="center"> <tr> <td height="47" width="191"> <div align="center"></div> </td> <td height="47" width="10"> <p align="center">&nbsp;</p> </td> <td height="47" width="556"> <p><font size="5"><b><font color="#FFFFFF">Colin G. Nichols, Ph.D.</font></b></font></p> </td> </tr> <tr> <td valign=top width="191" height="150"> <font color="#FFFFFF"> <p align=center><img src="../images/faculty/nichols.jpg" width="170" height="211"> </p> <p align=center><font size="+1">Washington University<br> School of Medicine</font></p> <p>Dept. of Cell Biology & Physiology<br> Box 8228<br> 660 S. Euclid Ave.<br> St. Louis, MO 63110</p> <p>tel: (314) <font size="+1">362-6630</font><br> fax: (314) <font size="+1">362-7463</font><br> email: <a href="mailto:cnichols@wustl.edu"><font color="#FFFFFF">cnichols@wustl.edu</font></a><br> <font color="#FFFFFF">web: <a href="http://www.nicholslab.wustl.edu/nichols.htm"><font color="#FFFFFF">Personal Weblink</font></a></font></p> <p>&nbsp; </p></font> </td> <td width="10" height="385">&nbsp;</td> <td width="556" height="385"> <p><font color="#FFFFFF"><b><font color="#FFFF00">RESEARCH INTEREST</font></b> </font></p> <p align="justify"><font color="#FFFFFF">A major goal of our efforts is to understand nutrient regulation of pancreatic hormone secretion, particularly the role of metabolism-excitation coupling via the ATP-sensitive K+ (KATP) channel. We are using gene manipulation approaches to understand the role of KATP channels as critical regulators of the link between nutrient levels and insulin secretion and our recent efforts have confirmed the central role of KATP channels in linking blood glucose levels to the secretion of insulin from pancreatic &beta;-cells, and mechanisms by which KATP channel disorders can lead to diabetes or hyperinsulinemia. Of relevance to the GI field, there is currently some controversy over whether such channels are present in gut L-cells, and whether they are involved in control of GLP secretion. It is our long-term hope that we may inform these issues by transgenic manipulation in vivo.</font></p> <p><font color="#FFFF00"><b>SELECTED PUBLICATIONS</b></font></p> <font color="#FFFFFF"> <p>1. Nichols, C.G., Shyng, S-L., Nestorowicz, A., Glaser, B., Clement, J.P. IV, Gonzales, G., Aguilar-Bryan, L., Permutt, A.M. and Bryan, J. (1996). Adenosine diphosphate as an intracellular regulator of insulin secretion. Science 272, 1785-1787.</p> <p>2. Shyng, S.-L. and Nichols, C.G. (1998). Phosphatidyl inositol phosphates control of nucleotide-sensitivity of KATP channels Science. 282, 1138-1141.</p> <p>3. Koster, J.C., B.A. Marshall, N. Ensor, J.A. Corbett and C.G. Nichols (2000). Targeted Overactivity of &beta;-cell KATP Channels Induces Profound Neonatal Diabetes. Cell 100, 645-654.</p> <p>4. Koster, J.C., M.S. Remedi, T. Flagg, J. Johnson, K. Markova, B.A. Marshall &amp; C.G. Nichols. (2002). Persistent hyperinsulinism induced by targeted suppression of &beta;-cell KATP channels. Proc. Natl. Acad. Sci. USA 99, 16992-16997.</p> <p>5. Remedi, M.S., J.C. Koster, K. Markova, S. Seino, T. Miki, B. Patton, M. McDaniel and C.G. Nichols (2004). Diet-induced glucose intolerance in mice with decreased beta-cell ATP-sensitive K+ channels. Diabetes 53, 3159-3167.</p> <p>6. Remedi, M.S., J.C. Koster, B. Patton, M. McDaniel and C.G. Nichols (2005). ATP-Sensitive K+ Channel Signaling in Glucokinase-Deficient Diabetes. Diabetes 54, 2925 2931.</p> <p>7. Koster, J.C., M.A. Permutt and C.G. Nichols (2005). Diabetes and insulin secretion: the KATP connection. Diabetes 54, 3065-3072.</p> <p>8. Koster, J.C., M.S. Remedi, R. Masia, B. Patton, A. Tong and C.G. Nichols (2006) Expression of ATP-Insensitive KATP Channels in Pancreatic {beta}-Cells Underlies a Spectrum of Diabetic Phenotypes. Diabetes 55, 2957-64.</p> <p>&nbsp;</p> </font> </td> </tr> </table> <h1>&nbsp;</h1> <h1>&nbsp;</h1> <h1><font size="+1"><BR> </font></h1> </body></html>