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1 Department of Surgery, University of Sydney, and 2 The Kolling Institute of Medical Research, Royal North Shore Hospital, Sydney, New South Wales 2065, Australia
Our aim was to
investigate the effects of modifying the carbohydrate-to-lipid ratio of
parenteral nutrition (PN) on body composition and the anabolic actions
of insulin-like growth factor I (IGF-I) and growth hormone (GH).
Adolescent male Sprague-Dawley rats were randomized to receive 7 days
of GH, IGF-I (3.5 mg · kg
1 · day
1 for both)
or placebo while receiving high-carbohydrate PN (CHO-PN), high-lipid PN
(L-PN), or an oral diet (chow) (the PN protocols were isonitrogenous
and isocaloric). PN impaired muscle growth, which was reversed by GH in
the CHO-PN group only (P < 0.03). PN increased carcass
lipid (P < 0.02), the effect being greater in the L-PN
than in the CHO-PN group (P < 0.001). Visceral lean tissue growth was significantly impaired by PN (P < 0.001). IGF-I reversed this impairment, but GH had no effect. PN
impaired the normal increase in hepatic protein and DNA
(P < 0.001) and produced liver steatosis
(P < 0.001). However, this steatosis was less in L-PN
than in CHO-PN (P < 0.001). Serum IGF-I and the
acid-labile subunit (ALS) were decreased by PN (P < 0.001) and were not affected by GH during PN treatment. However, GH
significantly increased serum ALS concentrations in the chow-fed rats
(P = 0.032). In conclusion, modifying the CHO-to-L
ratio of PN had no significant effect on IGF-I action, but CHO-PN
increased the peripheral effect of GH. L-PN increased carcass lipid
significantly and decreased hepatic steatosis. Nevertheless, PN caused
significant liver steatosis and profound impairment of hepatic cell
growth, which was associated with relative hepatic GH resistance.
growth hormone; parenteral nutrition; organ composition; body composition; insulin-like growth factor I treatment; steatosis; liver impairment
This article has been cited by other articles:
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M. B. Gillingham, E. M. Dahly, S. G. Murali, and D. M. Ney IGF-I treatment facilitates transition from parenteral to enteral nutrition in rats with short bowel syndrome Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2003; 284(2): R363 - R371. [Abstract] [Full Text] [PDF] |
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