AJP - GI AJP: Cell Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 270: G14-G19, 1996;
0193-1857/96 $5.00
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fried, R.
Right arrow Articles by Seelig, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fried, R.
Right arrow Articles by Seelig, J.

AJP - Gastrointestinal and Liver Physiology, Vol 270, Issue 1 14-G19, Copyright © 1996 by American Physiological Society


ARTICLES

Early glycogenolysis and late glycogenesis in human liver after intravenous administration of galactose

R. Fried, N. Beckmann, U. Keller, R. Ninnis, G. Stalder and J. Seelig
Department of Internal Medicine, University Hospital, Basel, Switzerland.

Galactose is incorporated by a different metabolic pathway than glucose. Its contribution to glycogen synthesis has not been studied in humans. We administered galactose (0.5 g/kg iv) to overnight-fasted normal human volunteers and examined its effects on hepatic glycogen synthesis and hepatic glucose output (HGO). Hepatic glycogenesis was assessed noninvasively, determining glycogen concentration by 13C magnetic resonance spectroscopy (MRS) and liver volume by magnetic resonance imaging. HGO was determined by [6,6-2H2]glucose and gluconeogenesis calculated by adding the amount of hepatic glycogenesis to the HGO. After galactose administration, liver glycogen concentration (baseline 254 +/- 11 mmol/l) decreased in the first 45 min to 207 +/- 15 mmol/l (P < 0.05) and increased thereafter to 313 +/- 7 mmol/l (P < 0.01). Net hepatic glycogenesis was 101 +/- 12 mmol over 150 min. HGO (baseline 14.3 +/- 1.9 mumol.kg-1.min-1) increased threefold in the first 15 min and then returned to baseline. The average rate of gluconeogenesis was 12.3 mumol.kg-1.min-1. Intravenous galactose leads to an increase in hepatic glycogen and hepatic glucose output in normal humans. Competitive inhibition of UDP-glucose pyrophosphorylase by UDP-galactose could explain the apparent glycogenolysis observed early after galactose administration. 13C MRS in combination with a stable isotope tracer is a noninvasive and safe method to study hepatic carbohydrate metabolism in humans.


This article has been cited by other articles:


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
P. Staehr, O. Hother-Nielsen, H. Beck-Nielsen, M. Roden, H. Stingl, J. J. Holst, P. K. Jones, V. Chandramouli, and B. R. Landau
Hepatic autoregulation: response of glucose production and gluconeogenesis to increased glycogenolysis
Am J Physiol Endocrinol Metab, May 1, 2007; 292(5): E1265 - E1269.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
V. Chandramouli, K. Ekberg, W. C. Schumann, S. C. Kalhan, J. Wahren, and B. R. Landau
Quantifying gluconeogenesis during fasting
Am J Physiol Endocrinol Metab, December 1, 1997; 273(6): E1209 - E1215.
[Abstract] [Full Text] [PDF]




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