Key result
Dystrophic hamsters exhibited altered glucose metabolism, with reduced age-related decline in sugar transport in fast-twitch muscle and greatly increased hexokinase activity in slow-twitch muscle.
May warrant investigation of muscle glucose metabolism in human dystrophy; leaves open whether metabolic modulation alters progression.
The facilitated diffusion system for monosaccharides was studied with nonmetabolized 3-O-methyl-D-glucose (3-O-MG) and hexokinase activity was determined with 2-deoxyglucose (2-DG) in extensor digitorum longus (EDL) and soleus muscles from BIO 14.6 (dystrophic) hamsters. Motor activity was recorded at 2 months of age. F1B (normal) hamsters were controls. In EDL (fast-twitch) muscle, sugar transport was unaltered at 6 weeks; at 2 to 5 months the normal decrease in sugar transport with time was reduced, decreasing stimulation of the facilitated diffusion system by anoxia. Phosphorylation in EDL muscles, measured at 2 months, probably was decreased. In soleus (slow-twitch) muscle, 3-O-MG transport was unaltered with age but hexokinase activity, determined at 2 months, was greatly increased in the quiescent state and during stimulation at 2 Hz. Motor activity was less, but not significantly, in the dystrophic hamsters. The results indicate that the alterations in glucose metabolism depend upon both muscle type and age. We interpret the changes in dystrophic fast- and slow-twitch muscles as reflecting compensatory mechanisms to increase the generation of energy.
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Phipps et al. (1983) studied Cardiomyopathy. BIO 14.6 (dystrophic) strain vs. F1B (normal) hamsters was evaluated on Monosaccharide transport and hexokinase activity. Dystrophic hamsters exhibited altered glucose metabolism, with reduced age-related decline in sugar transport in fast-twitch muscle and greatly increased hexokinase activity in slow-twitch muscle.
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