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Am J Physiol Endocrinol Metab 276: E435-E442, 1999;
0193-1849/99 $5.00
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Vol. 276, Issue 3, E435-E442, March 1999

Decreased hexosamine biosynthesis in GH-deficient dwarf rat muscle. Reversal with GH, but not IGF-I, therapy

Katherine A. Robinson1, Steven M. Willi2, Sarah Bingel3, and Maria G. Buse1,4

1 Division of Endocrinology, Diabetes, and Medical Genetics, Department of Medicine, and Departments of 2 Pediatrics, 3 Laboratory Animal Resources, and 4 Biochemistry/Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425-2222

Enhanced glucose flux via the hexosamine biosynthesis pathway (HNSP) has been implicated in insulin resistance. We measured L-glutamine:D-fructose-6-phosphate amidotransferase activity (GFAT, a rate-limiting enzyme) and concentrations of UDP-N-acetyl hexosamines (UDP-HexNAc, major products of HNSP) in muscle and liver of growth hormone (GH)-deficient male dwarf (dw) rats. All parameters measured, except body weight, were similar in 5-wk-old control and dw rats. Muscle GFAT activity declined progressively with age in controls and dw rats but was consistently 30-60% lower in 8- to 14-wk-old dw rats vs. age-matched controls; UDP-HexNAc concentrations in muscle were concomitantly 30% lower in dw rats vs. controls (P < 0.01). Concentrations of UDP-hexoses, GDP-mannose, and UDP in muscle were similar in control and dw rats. Muscle HNSP activity was similarly diminished in fed and fasted dw rats. In liver, only a small difference in GFAT activity was evident between controls and dw rats, and no differences in UDP-HexNAc concentrations were observed. Treatment with recombinant human GH (rhGH) for 5 days restored UDP-HexNAc to control levels in dw muscles (P < 0.01) and partially restored GFAT activity. Insulin-like growth factor I treatment was ineffective. We conclude that GH participates in HNSP regulation in muscle.

L-glutamine:D-fructose-6-phosphate amidotransferase activity in muscle and liver; UDP-N-acetyl hexosamine concentration in muscle and liver; regulation of hexosamine biosynthesis by growth hormone in muscle; growth hormone-induced insulin resistance


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