J. Biol. Chem., Vol. 264, Issue 1, 168-172, 01, 1989
Glucose phosphorylation is not rate limiting for accumulation of glycogen from glucose in perfused livers from fasted rats
JH Youn, M Ader and RN Bergman
Department of Physiology and Biophysics, University of Southern California Medical School, Los Angeles 90033.
Incorporation of Glc and Fru into glycogen was measured in perfused livers
from 24-h fasted rats using [6-3H]Glc and [U-14C]Fru. For the initial 20
min, livers were perfused with low Glc (2 mM) to deplete hepatic glycogen
and were perfused for the following 30 min with various combinations of Glc
and Fru. With constant Fru (2 mM), increasing perfusate Glc increased the
relative contribution of Glc carbons to glycogen (7.2 +/- 0.4, 34.9 +/-
2.8, and 59.1 +/- 2.7% at 2, 10, and 20 mM Glc, respectively; n = 5 for
each). During perfusion with substrate levels seen during refeeding (10 mM
Glc, 1.8 mumol/g/min gluconeogenic flux from 2 mM Fru), Fru provided 54.7
+/- 2.7% of the carbons for glycogen, while Glc provided only 34.9 +/-
2.8%, consistent with in vivo estimations. However, the estimated rate of
Glc phosphorylation was at least 1.10 +/- 0.11 mumol/g/min, which exceeded
by at least 4-fold the glycogen accumulation rate (0.28 +/- 0.04 mumol of
glucose/g/min). The total rate of glucose 6-phosphate supply via Glc
phosphorylation and gluconeogenesis (2.9 mumol/g/min) exceeded reported in
vivo rates of glycogen accumulation during refeeding. Thus, in perfused
livers of 24-h fasted rats there is an apparent redundancy in glucose
6-phosphate supply. These results suggest that the rate- limiting step for
hepatic glycogen accumulation during refeeding is located between glucose
6-phosphate and glycogen, rather than at the step of Glc phosphorylation or
in the gluconeogenic pathway.
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