Insulin-like growth factor i inhibits degradation and improves
retention of protein in hind limb muscle of lambs.
Oddy, V. Hutton, and Phillip C. Owens.
Elizabeth Macarthur Agricultural Institute, New South Wales
Agriculture, Camden, New South Wales, 2570, Australia, and
Cooperative Research Centre for Tissue Growth and Repair,
Commonwealth Scientific and Industrial Research Organization,
Division of Human Nutrition, Adelaide, South Australia 8000,
Australia
APStracts 3:0156E, 1996.
We infused recombinant human IGF-1 for 4 h at 12.3 [mu]g/h per kg live
weight directly into the left femoral artery and measured the rates
of synthesis, degradation and gain of protein by the treated and
contra lateral limbs of well fed (n=8), feed restricted (n=10) and
fasted (n=9) castrate male lambs. Reducing feed intake decreased net
protein gain of hind limb muscle, reduced hind limb glucose uptake
and lowered arterial plasma concentrations of IGF-1, insulin,
glucose, phenylalanine, tyrosine and isoleucine. The effect of
nutrition on IGF-binding proteins (IGFBPs) was generally small,
IGFBP-2 was more abundant in fasted lambs. Infusion of IGF-1 into the
left femoral artery increased plasma levels of IGF-1 two- to four
-fold in the left femoral vein and by 1.5- to three-fold in the artery
and right femoral vein. In the treated limb, IGF-1 reduced protein
degradation, increased protein gain and increased glucose uptake
without altering blood flow or oxygen uptake, regardless of feed
intake. Systemically, IGF-1 reduced plasma insulin, phenylalanine,
tyrosine, isoleucine and leucine in all nutrition groups. Plasma
IGFBP-3 was increased by 4 h of IGF-1 treatment in fasted but not in
fed lambs. In fed, but not fasted lambs, IGF-1 increased blood
glucose concentration. Effects of IGF-1 on protein metabolism in the
contra lateral limb were affected by nutrition, and generally larger
in fasted than in unrestricted fed lambs.
Received 16 January 1996; accepted in final form 26 July 1996.
APS Manuscript Number E20-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996