| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
AJP - Cell Physiology, Vol 266, Issue 3 C622-C627, Copyright © 1994 by American Physiological Society
ARTICLES |
T. Aizawa, Y. Sato, F. Ishihara, N. Taguchi, M. Komatsu, N. Suzuki, K. Hashizume and T. Yamada
Department of Geriatrics, Endocrinology and Metabolism, Shinshu University School of Medicine, Nagano-ken, Japan.
The nature of ATP-sensitive K+ (K+ATP) channel-independent, insulinotropic action of glucose was investigated using non-glucose-primed pancreatic islets. When the beta-cell was depolarized with K+, glucose dose dependently stimulated insulin release despite inhibition of the K+ATP channel closure by diazoxide. K+ depolarization could be replaced with BAY K 8644, a calcium channel agonist. Prior fasting of rats and lowering ambient temperature greatly suppressed glucose oxidation and utilization by the islet cells and abolished insulin release in response to high glucose alone. However, under these conditions, the K+ATP channel-independent, glucose-induced insulin release was clearly demonstrable. p-Nitrophenyl-alpha-D-glucopyranoside (sweet taste inhibitor) but not its beta-isomer, neomycin (phospholipase C inhibitor) and staurosporine (C kinase blocker) inhibited the K+ATP channel-independent, insulinotropic action of glucose. For the K+ATP channel-independent glucose-induced insulin release 1) elevation of cytosolic calcium is required, 2) minute glucose metabolism is enough, if glucose metabolism is necessary, and 3) direct recognition of glucose molecule, phospholipase C, and protein kinase C appear to be involved.
This article has been cited by other articles:
|
|
 |
|
  S. G. Straub and G. W. G. Sharp Hypothesis: one rate-limiting step controls the magnitude of both phases of glucose-stimulated insulin secretion Am J Physiol Cell Physiol, September 1, 2004; 287(3): C565 - C571. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Geng, L. Li, S. Watkins, P. D. Robbins, and P. Drain The Insulin Secretory Granule Is the Major Site of KATP Channels of the Endocrine Pancreas Diabetes, March 1, 2003; 52(3): 767 - 776. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Noda, S. Yamashita, N. Takahashi, K. Eto, L.-M. Shen, K. Izumi, S. Daniel, Y. Tsubamoto, T. Nemoto, M. Iino, et al. Switch to Anaerobic Glucose Metabolism with NADH Accumulation in the beta -Cell Model of Mitochondrial Diabetes. CHARACTERISTICS OF beta HC9 CELLS DEFICIENT IN MITOCHONDRIAL DNA TRANSCRIPTION J. Biol. Chem., October 25, 2002; 277(44): 41817 - 41826. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. K. Bratanova-Tochkova, H. Cheng, S. Daniel, S. Gunawardana, Y.-J. Liu, J. Mulvaney-Musa, T. Schermerhorn, S. G. Straub, H. Yajima, and G. W.G. Sharp Triggering and Augmentation Mechanisms, Granule Pools, and Biphasic Insulin Secretion Diabetes, February 1, 2002; 51(90001): S83 - 90. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Aizawa, Y. Sato, and M. Komatsu Importance of Nonionic Signals for Glucose-Induced Biphasic Insulin Secretion Diabetes, February 1, 2002; 51(90001): S96 - 98. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Eto, T. Yamashita, Y. Tsubamoto, Y. Terauchi, K. Hirose, N. Kubota, S. Yamashita, J. Taka, S. Satoh, H. Sekihara, et al. Phosphatidylinositol 3-Kinase Suppresses Glucose-Stimulated Insulin Secretion by Affecting Post-Cytosolic [Ca2+] Elevation Signals Diabetes, January 1, 2002; 51(1): 87 - 97. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Anello, V. Ucciardello, S. Piro, G. Patane, L. Frittitta, V. Calabrese, A. M. Giuffrida Stella, R. Vigneri, F. Purrello, and A. M. Rabuazzo Chronic exposure to high leucine impairs glucose-induced insulin release by lowering the ATP-to-ADP ratio Am J Physiol Endocrinol Metab, November 1, 2001; 281(5): E1082 - E1087. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Fujimoto, Y. Tsuura, H. Ishida, K. Tsuji, E. Mukai, M. Kajikawa, Y. Hamamoto, T. Takeda, Y. Yamada, and Y. Seino Augmentation of basal insulin release from rat islets by preexposure to a high concentration of glucose Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E927 - E940. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Eto, S. Suga, M. Wakui, Y. Tsubamoto, Y. Terauchi, J. Taka, S. Aizawa, M. Noda, S. Kimura, H. Kasai, et al. NADH Shuttle System Regulates KATP Channel-dependent Pathway and Steps Distal to Cytosolic Ca2+ Concentration Elevation in Glucose-induced Insulin Secretion J. Biol. Chem., September 3, 1999; 274(36): 25386 - 25392. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. G. Xu, Z.-y. Gao, P. D. Borge Jr., and B. A. Wolf Insulin Receptor Substrate 1-induced Inhibition of Endoplasmic Reticulum Ca2+ Uptake in beta -Cells. AUTOCRINE REGULATION OF INTRACELLULAR Ca2+ HOMEOSTASIS AND INSULIN SECRETION J. Biol. Chem., June 18, 1999; 274(25): 18067 - 18074. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Takahashi, T. Kadowaki, Y. Yazaki, G. C. R. Ellis-Davies, Y. Miyashita, and H. Kasai Post-priming actions of ATP on Ca2+-dependent exocytosis in pancreatic beta cells PNAS, January 19, 1999; 96(2): 760 - 765. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
