help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lee, B.
Right arrow Articles by Laychock, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, B.
Right arrow Articles by Laychock, S. G.
Endocrinology Vol. 140, No. 5 2173-2182
Copyright © 1999 by The Endocrine Society

ARTICLES

Glucose Regulates Expression of Inositol 1,4,5-Trisphosphate Receptor Isoforms in Isolated Rat Pancreatic Islets1

Bumsup Lee2, Jean-Christophe Jonas3, Gordon C. Weir and Suzanne G. Laychock

Department of Pharmacology and Toxicology (B.L., S.G.L.), School of Medicine and Biomedical Sciences, the State University of New York at Buffalo, Buffalo, New York 14214; and the Research Division (J.-C.J., G.C.W.), Joslin Diabetes Center, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215

Address all correspondence and requests for reprints to: Dr. Suzanne Laychock, 102 Farber Hall, State University of New York at Buffalo, School of Medicine, Buffalo, New York 14214. E-mail: laychock{at}acsu.buffalo.edu

Isolated rat pancreatic islets were studied to determine the dynamic regulatory effects of glucose stimulation on the expression of messenger RNA (mRNA) and protein levels for inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) isoforms I, II, and III. The relative isoform abundance was: IP3R-III > IP3R-II ~ IP3R-I. Culture of islets with glucose (G; 20 mM) or {alpha}-ketoisocaproic acid for 30 min increased only IP3R-III mRNA expression above control (5.5 mM glucose). 2-Deoxyglucose was without effect. Islet culture for 2 h with G (20 mM) or {alpha}-ketoisocaproic acid reduced IP3R-III mRNA expression levels below control, and cycloheximide blocked the response. Culturing islets for 1 day or 7 days with G (11 mM) reduced the expression of IP3R-III mRNA but increased the expression of IP3R-II mRNA in a time-dependent manner. Cytosine arabinoside lowered cultured islet IP3R-II and -III mRNA levels, but glucose effects remained evident. IP3R-II mRNA levels were also significantly higher in islets from hyperglycemic 90% partial pancreatectomized rats, compared with sham animals. Islet IP3R mRNA expression also showed osmotic sensitivity. Islet IP3R-III protein levels increased after 2 h islet culture at 20 mM G, were unchanged after 1 day culture at 11 mM G, and were lower than control after 7 days culture at 11 mM G. In contrast, IP3R-II levels increased after 1 day and 7 days culture at 11 mM G, whereas IP3R-I protein levels remained unchanged. Thus, G stimulation rapidly increases transcription and expression of IP3R-III mRNA and protein levels in rat islets. However, chronic G stimulation up-regulates IP3R-II mRNA in cultured islets and in islets from partial pancreatectomized rats. Metabolic regulation of IP3R-II and III expression may mediate ß-cell IP3-responsive Ca2+ mobilization and insulin secretion.




This article has been cited by other articles:


Home page
 DiabetesHome page
D. S. Luciani, K. S. Gwiazda, T.-L. B. Yang, T. B. Kalynyak, Y. Bychkivska, M. H.Z. Frey, K. D. Jeffrey, A. V. Sampaio, T. M. Underhill, and J. D. Johnson
Roles of IP3R and RyR Ca2+ Channels in Endoplasmic Reticulum Stress and {beta}-Cell Death
Diabetes, February 1, 2009; 58(2): 422 - 432.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
S. G. Laychock, Y. Tian, and S. M. Sessanna
Endothelial Differentiation Gene Receptors in Pancreatic Islets and INS-1 Cells
Diabetes, August 1, 2003; 52(8): 1986 - 1993.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
P. Gilon and J.-C. Henquin
Mechanisms and Physiological Significance of the Cholinergic Control of Pancreatic {beta}-Cell Function
Endocr. Rev., October 1, 2001; 22(5): 565 - 604.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
B. Lee, W. Gai, and S. G. Laychock
Proteasomal Activation Mediates Down-Regulation of Inositol 1,4,5-Trisphosphate Receptor and Calcium Mobilization in Rat Pancreatic Islets
Endocrinology, May 1, 2001; 142(5): 1744 - 1751.
[Abstract] [Full Text]

Home page
 Circ. Res.Home page
Y. Wang, J. Chen, Y. Wang, C. W. Taylor, Y. Hirata, H. Hagiwara, K. Mikoshiba, T. Toyo-oka, M. Omata, and Y. Sakaki
Crucial Role of Type 1, but Not Type 3, Inositol 1,4,5-Trisphosphate (IP3) Receptors in IP3-Induced Ca2+ Release, Capacitative Ca2+ Entry, and Proliferation of A7r5 Vascular Smooth Muscle Cells
Circ. Res., February 2, 2001; 88(2): 202 - 209.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
A. Tengholm, B. Hellman, and E. Gylfe
The endoplasmic reticulum is a glucose-modulated high-affinity sink for Ca2+ in mouse pancreatic {beta}-cells
J. Physiol., February 1, 2001; 530(3): 533 - 540.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
B. Lee and S. G. Laychock
Regulation of Inositol Trisphosphate Receptor Isoform Expression in Glucose-Desensitized Rat Pancreatic Islets: Role of Cyclic Adenosine 3',5'-Monophosphate and Calcium
Endocrinology, April 1, 2000; 141(4): 1394 - 1402.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1999 by The Endocrine Society