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Am J Physiol Gastrointest Liver Physiol 272: G374-G382, 1997;
0193-1857/97 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 272, Issue 2 374-G382, Copyright © 1997 by American Physiological Society

ARTICLES

Progressive defect in biliary GSH secretion in streptozotocin-induced diabetic rats

S. C. Lu, J. Kuhlenkamp, H. Wu, W. M. Sun, L. Stone and N. Kaplowitz
Department of Medicine, University of Southern California School of Medicine, and the Department of Veteran Affairs Outpatient Clinic, Los Angeles 90033, USA.

This study examined the effect of streptozotocin-induced diabetes on biliary reduced glutathione (GSH) efflux. Biliary GSH efflux was measured before and after acivicin, an irreversible inhibitor of gamma-glutamyl transpeptidase (GGT). One week after streptozotocin treatment, liver GGT activity doubled in diabetic rats but was inhibited by approximately 90% after acivicin to levels comparable to controls. Despite maximal GGT inhibition, biliary GSH efflux in untreated diabetic rats decreased progressively to approximately 10% of control levels by week 4 and was partially restored by insulin. The mechanism for the decrease in biliary GSH efflux was not increased paracellular permeability. GSH transport kinetics, ATP-stimulated taurocholate, and oxidized glutathione (GSSG) transport in canalicular liver plasma membrane prepared from diabetic and control rats were similar. Inhibition of protein kinase C (PKC) with high-dose H-7 increased biliary GSH efflux in diabetic animals to near control basal levels. In conclusion, streptozotocin-induced diabetic rats exhibit a progressive impairment in biliary GSH transport. One of the responsible mechanisms is heightened PKC tone in diabetic animals.


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A. V. Mittur, N. Kaplowitz, E. S. Kempner, and M. Ookhtens
Novel properties of hepatic canalicular reduced glutathione transport revealed by radiation inactivation
Am J Physiol Gastrointest Liver Physiol, May 1, 1998; 274(5): G923 - G930.
[Abstract] [Full Text] [PDF]


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