Regulation of hexokinase ii activity and expression in human muscle
by moderate exercise.
Koval, Janice A., Ralph A. Defronzo, Robert M. Oaedoherty, Richard
Printz, Hossein Ardehali, Daryl K. Granner, and Lawrence J.
Mandarino.
Division of Diabetes, Department of Medicine and the Department of
Biochemistry, The University of Texas Health Science Center at San
Antonio, San Antonio, Texas; the Department of Molecular Physiology
and Biophysics, Vanderbilt University School of Medicine, Nashville,
Tennessee 37232-0615
APStracts 4:0251E, 1997.
A single bout of exercise increases the rate of insulin-stimulated
glucose uptake and metabolism in skeletal muscle. Exercise also
increases insulin-stimulated glucose 6-phosphate in skeletal muscle,
suggesting that exercise increases hexokinase activity. Within three
hours, exercise increases hexokinase II (HK II) mRNA and activity in
skeletal muscle from rats. It is not known, however, if a single bout
of moderate intensity exercise increases HKII expression in humans.
The present study was undertaken to answer this question. Six
subjects had percutaneous biopsies of the vastus lateralis muscle
before and three hours after a single one hour session of moderate
intensity, aerobic (60% of VO2max) exercise. Glycogen synthase, HKI,
and HKII activities as well as HKI and HKII mRNA content were
determined from the muscle biopsy specimens. The fractional velocity
of glycogen synthase was increased by 446 ( 84 % after exercise (P
< 0.005). Hexokinase II activity in the soluble fraction of the
homogenates increased from 1.2 ( 0.4 to 4.5 ( 1.6 pmole/min.(g (P <
0.05) but was unchanged in the particulate fraction (4.3 ( 1.3 vs.
5.3 ( 1.5). Hexokinase I activity in neither the soluble nor
particulate fraction changed after exercise. Relative to a 28S rRNA
control signal, HKII mRNA increased from 0.091 ( 0.02 to 0.195 (
0.037 (P < 0.05), while HKI mRNA was unchanged (0.414 ( 0.061 vs.
0.498 ( 0.134, P < 0.20). The increase in HKII activity after
moderate exercise in healthy subjects could be one factor responsible
for the enhanced rate of insulin-stimulated glucose uptake seen
following exercise.
Received 4 August 1997; accepted in final form 6 November 1997.
APS Manuscript Number E364-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 14 November 1997