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1 Department of Medicine V and
2 Institute of Experimental
Clinical Research,
Growth hormone (GH) reduces the catabolic side effects of
steroid treatment due to its effects on tissue protein
synthesis/degradation. Little attention is focused on hepatic amino
acid degradation and urea synthesis. Five groups of rats were given
1) placebo, 2) prednisolone,
3) placebo, pair fed to the steroid
group, 4) GH, and
5) prednisolone and GH. After 7 days, the in vivo capacity of urea N synthesis (CUNS) was determined by
saturating alanine infusion, in parallel with measurements of liver
mRNA levels of urea cycle enzymes, N contents of organs, N balance, and
hormones. Prednisolone increased CUNS
(µmol · min
1 · 100 g1, mean ± SE) from 9.1 ± 1.0 (pair-fed controls) to 13.2 ± 0.8 (P < 0.05), decreased basal blood
-amino N concentration from 4.2 ± 0.5 to 3.1 ± 0.3 mmol/l
(P < 0.05), increased mRNA levels of
the rate- and flux-limiting urea cycle enzymes by 20 and 65%, respectively (P < 0.05), and
decreased muscle N contents and N balance. In contrast, GH decreased
CUNS from 6.1 ± 0.9 (free-fed controls) to 4.2 ± 0.5 (P < 0.05), decreased basal blood
-amino N concentration from 3.8 ± 0.3 to 3.2 ± 0.2, decreased mRNA levels of the rate- and flux-limiting urea cycle enzymes
to 60 and 40%, respectively (P < 0.05), and increased organ N contents and N balance. Coadministration
of GH abolished all steroid effects. We found that prednisolone
increases the ability of amino N conversion into urea N and urea cycle
gene expression. GH had the opposite effects and counteracted the
N-wasting side effects of prednisolone.
amino acid metabolism; liver; ureagenesis; messenger ribonucleic acid
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