Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 100: 150-156, 2006. First published September 15, 2005; doi:10.1152/japplphysiol.00988.2005
8750-7587/06 $8.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
100/1/150    most recent
00988.2005v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 ISI Web of Science
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 ISI Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ceylan-Isik, A. F.
Right arrow Articles by Ren, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ceylan-Isik, A. F.
Right arrow Articles by Ren, J.

High-dose benfotiamine rescues cardiomyocyte contractile dysfunction in streptozotocin-induced diabetes mellitus

Asli F. Ceylan-Isik,* Shan Wu,* Qun Li, Shi-Yan Li, and Jun Ren

Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, Wyoming

Submitted 15 August 2005 ; accepted in final form 12 September 2005

Diabetic cardiomyopathy is characterized by cardiac dysfunction. This study was designed to examine the effect of benfotiamine, a lipophilic derivative of thiamine, on streptozotocin (STZ)-induced cardiac contractile dysfunction in mouse cardiomyocytes. Adult male FVB mice were made diabetic with a single injection of STZ (200 mg/kg ip). Fourteen days later, control and diabetic (fasting plasma glucose > 13.9 mM) mice were put on benfotiamine therapy (100 mg·kg–1·day–1 ip) for another 14 days. Mechanical and intracellular Ca2+ properties were evaluated in left ventricular myocytes using an IonOptix MyoCam system. The following indexes were evaluated: peak shortening (PS), time to PS (TPS), time to 90% relengthening (TR90), maximal velocity of shortening/relengthening, resting and rise of intracellular Ca2+ in response to electrical stimulus, sarcoplasmic reticulum (SR) Ca2+ load, and intracellular Ca2+ decay rate ({tau}). Two- or four-week STZ treatment led to hyperglycemia, prolonged TPS and TR90, reduced SR Ca2+ load, elevated resting intracellular Ca2+ level and prolonged {tau} associated with normal PS, maximal velocity of shortening/relengthening, and intracellular Ca2+ rise in response to electrical stimulus. Benfotiamine treatment abolished prolongation in TPS, TR90, and {tau}, as well as reduction in SR Ca2+ load without affecting hyperglycemia and elevated resting intracellular Ca2+. Diabetes triggered oxidative stress, measured by GSH-to-GSSG ratio and formation of advanced glycation end product (AGE) in the hearts. Benfotiamine treatment alleviated oxidative stress without affecting AGE or protein carbonyl formation. Collectively, our results indicated that benfotiamine may rescue STZ-induced cardiomyocyte dysfunction but not AGE formation in short-term diabetes.

diabetes; ventricular myocyte; contraction; advanced glycation end product


Address for reprint requests and other correspondence: J. Ren, Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, Univ. of Wyoming, Laramie, WY 82071 (e-mail: jren{at}uwyo.edu)




This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
C. Tikellis, M. C. Thomas, B. E. Harcourt, M. T. Coughlan, J. Pete, K. Bialkowski, A. Tan, A. Bierhaus, M. E. Cooper, and J. M. Forbes
Cardiac inflammation associated with a Western diet is mediated via activation of RAGE by AGEs
Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E323 - E330.
[Abstract] [Full Text] [PDF]

Home page
 J CARDIOVASC PHARMACOL THERHome page
M. J. Crespo, J. Zalacain, D. C. Dunbar, N. Cruz, and L. Arocho
Cardiac Oxidative Stress Is Elevated at the Onset of Dilated Cardiomyopathy in Streptozotocin-Diabetic Rats
Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2008; 13(1): 64 - 71.
[Abstract] [PDF]

Home page
 Circ. Res.Home page
W. Hsueh, E. D. Abel, J. L. Breslow, N. Maeda, R. C. Davis, E. A. Fisher, H. Dansky, D. A. McClain, R. McIndoe, M. K. Wassef, et al.
Recipes for Creating Animal Models of Diabetic Cardiovascular Disease
Circ. Res., May 25, 2007; 100(10): 1415 - 1427.
[Abstract] [Full Text] [PDF]

Home page
 PhysiologyHome page
S. Boudina and E. D. Abel
Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes.
Physiology, August 1, 2006; 21: 250 - 258.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
V. Marchetti, R. Menghini, S. Rizza, A. Vivanti, T. Feccia, D. Lauro, A. Fukamizu, R. Lauro, and M. Federici
Benfotiamine Counteracts Glucose Toxicity Effects on Endothelial Progenitor Cell Differentiation via Akt/FoxO Signaling.
Diabetes, August 1, 2006; 55(8): 2231 - 2237.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.