AJP - Endo Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab 275: E1055-E1060, 1998;
0193-1849/98 $5.00
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sánchez-Margalet, V.
Right arrow Articles by González-Yanes, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sánchez-Margalet, V.
Right arrow Articles by González-Yanes, C.
Vol. 275, Issue 6, E1055-E1060, December 1998

Pancreastatin inhibits insulin action in rat adipocytes

Víctor Sánchez-Margalet and Carmen González-Yanes

Department of Medical Biochemistry and Molecular Biology, School of Medicine, Investigation Unit of the University Hospital Virgen Macarena, Seville 41009, Spain

Pancreastatin (PST), a regulatory peptide with a general inhibitory effect on secretion, is derived from chromogranin A, a glycoprotein present throughout the neuroendocrine system. We have previously demonstrated the counterregulatory role of PST on insulin action in rat hepatocytes. Here, we are reporting the PST effects on rat adipocytes. PST dose dependently inhibits basal and insulin-stimulated glucose transport, lactate production, and lipogenesis, impairing the main metabolic actions of insulin in adipocytes. These effects were observed in a wide range of insulin concentrations, leading to a shift to the right in the dose-response curve. Maximal effect was observed at 10 nM PST, and the IC50 value was ~1 nM. Moreover, PST has a lipolytic effect in rat adipocytes (ED50 0.1 nM), although it was completely inhibited by insulin. In contrast, PST dose dependently stimulated protein synthesis and enhanced insulin-stimulated protein synthesis. In summary, these data show the lipokinetic effect of PST and the inhibitory effect of PST on insulin metabolic action within a range of physiological concentrations. Therefore, these results give new pathophysiological basis for the association of PST with insulin resistance.

chromogranin A; peptide; metabolism; insulin resistance


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
J. R. Gayen, M. Saberi, S. Schenk, N. Biswas, S. M. Vaingankar, W. W. Cheung, S. M. Najjar, D. T. O'Connor, G. Bandyopadhyay, and S. K. Mahata
A Novel Pathway of Insulin Sensitivity in Chromogranin A Null Mice: A CRUCIAL ROLE FOR PANCREASTATIN IN GLUCOSE HOMEOSTASIS
J. Biol. Chem., October 16, 2009; 284(42): 28498 - 28509.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
C. Gonzalez-Yanes, A. Serrano, F. J. Bermudez-Silva, M. Hernandez-Dominguez, M. A. Paez-Ochoa, F. R. de Fonseca, and V. Sanchez-Margalet
Oleylethanolamide impairs glucose tolerance and inhibits insulin-stimulated glucose uptake in rat adipocytes through p38 and JNK MAPK pathways
Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E923 - E929.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online