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. 1993 Dec 15;296 ( Pt 3)(Pt 3):765-9.
doi: 10.1042/bj2960765.

Acute effects of insulin-like growth factor I on inter-organ amino acid flux in protein-catabolic dogs

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Acute effects of insulin-like growth factor I on inter-organ amino acid flux in protein-catabolic dogs

E Roth et al. Biochem J. .

Abstract

The effects of acute administration of human recombinant insulin-like growth factor-I (rhIGF-I) on amino acid (AA) flux between hindlimbs, liver and gut were investigated in anaesthetized post-operative dogs. rhIGF-I produced about a 10-fold increase in plasma IGF-I concentrations above baseline values (P < 0.001), increased the plasma levels of glucagon and adrenaline (P < 0.05), and evoked a fall in plasma glucose (-55 +/- 8%; (P < 0.001) and plasma total AA levels (-23 +/- 8%; P < 0.05). AA flux in post-absorptive dogs under NaCl infusions was characterized by an efflux of AA from the hindlimbs (as a result of the protein-catabolic situation), an equal AA balance across the gut and an AA uptake by the liver. The administration of rhIGF-I increased hepatic AA uptake in the NaCl group from 3.51 +/- 0.8 to 7.5 +/- 0.4 mumol/min per kg (P < 0.01) and in the AA-infused group from 16.8 +/- 0.6 to 22.4 +/- 1.5 mumol/min per kg (P < 0.05), but did not influence the AA balance across hindlimbs and gut. Glucose infusions normalized the plasma concentrations of counter-regulatory hormones without influencing the inter-organ AA balances. We conclude that hypoaminoacidaemia caused by rhIGF-I infusions is the result of a stimulated AA uptake by the liver, but is unrelated to alterations of AA exchange across the hindlimbs.

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References

    1. Physiol Rev. 1971 Jan;51(1):23-65 - PubMed
    1. Am J Physiol. 1989 Aug;257(2 Pt 1):E228-34 - PubMed
    1. Surgery. 1979 Sep;86(3):409-22 - PubMed
    1. Nature. 1982 Mar 18;296(5854):252-3 - PubMed
    1. Clin Chem. 1982 Mar;28(3):527-31 - PubMed

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