title: Parenteral nutrition with lipid or glucose suppresses liver growth and response to GH in adolescent male rats.
abstract: 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.
authors.affiliation: Department of Surgery, University of Sydney, Sydney, New South Wales 2065, Australia.
authors.forename: A
authors.initials: A
authors.lastname: Sevette
authors.forename: A J
authors.initials: AJ
authors.lastname: Kee
authors.forename: A R
authors.initials: AR
authors.lastname: Carlsson
authors.forename: R C
authors.initials: RC
authors.lastname: Baxter
authors.forename: R C
authors.initials: RC
authors.lastname: Smith
mesh_terms: D000818:Animals; D001823:Body Composition / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D004247:DNA / Q000378:metabolism; D004351:Drug Resistance; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005234:Fatty Liver / Q000209:etiology; D005947:Glucose / Q000008:administration & dosage*; D019382:Human Growth Hormone / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology; D050356:Lipid Metabolism; D008055:Lipids / Q000008:administration & dosage*; D008099:Liver / Q000187:drug effects* / Q000254:growth & development* / Q000378:metabolism; D010288:Parenteral Nutrition; D011506:Proteins / Q000378:metabolism; D051381:Rats
chemical_list: D005230:Fatty Acids, Nonesterified; D008055:Lipids; D011506:Proteins; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D004247:DNA; D005947:Glucose