FASEB J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kurland, I. J.
Right arrow Articles by Pilkis, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kurland, I. J.
Right arrow Articles by Pilkis, S. J.

The FASEB Journal, Vol 3, 2277-2281, Copyright © 1989 by The Federation of American Societies for Experimental Biology

REVIEWS

Indirect versus direct routes of hepatic glycogen synthesis

IJ Kurland and SJ Pilkis
Department of Physiology and Biophysics, State University of New York, Stony Brook 11794.

During refeeding after a brief period of starvation, glucose carbon is deposited into hepatic glycogen by both a direct and an indirect route. In the indirect route glucose is first metabolized to 3-carbon precursors, which then transverse the gluconeogenic pathway before being deposited into glycogen. Recent studies have yielded widely different estimates of the percentage of glucose carbon that follows the indirect route. Work summarized here demonstrates that the relative contributions of glucose carbon to hepatic glycogen formation by the indirect and direct pathways are greatly dependent on experimental design, and at least in vitro, are possibly dependent on the extent of glycogen/glucose 1-P recycling. Under physiological refeeding conditions in vivo, both pathways are used, each contributing approximately 50% of the amount of carbon appearing in glycogen. The level of glucokinase activity does not appear to be responsible for poor glucose utilization in liver. Poor glucose utilization in isolated liver preparations may result from the absence of a neurophysiological feedback loop that senses the arterial/portal glucose gradient and then regulates whole liver glucose uptake.


This article has been cited by other articles:


Home page
 DiabetesHome page
H. C. Murphy, G. Regan, I. G. Bogdarina, A. J.L. Clark, R. A. Iles, R. D. Cohen, G. A. Hitman, C. L. Berry, Z. Coade, C. J. Petry, et al.
Fetal Programming of Perivenous Glucose Uptake Reveals a Regulatory Mechanism Governing Hepatic Glucose Output During Refeeding
Diabetes, June 1, 2003; 52(6): 1326 - 1332.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Z. Guo and M. D. Jensen
Blood Glycerol Is an Important Precursor for Intramuscular Triacylglycerol Synthesis
J. Biol. Chem., August 20, 1999; 274(34): 23702 - 23706.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
H. Gunderson, N. Wehmeyer, D. Burnett, J. Nauman, C. Hartzell, and S. Savage
Exercise and exhaustion effects on glycogen synthesis pathways
J Appl Physiol, November 1, 1996; 81(5): 2020 - 2026.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by The Federation of American Societies for Experimental Biology.