Parenteral nutrition with lipid or glucose suppresses liver growth and response to GH in adolescent male rats

Am J Physiol Endocrinol Metab. 2001 Nov;281(5):E1063-72. doi: 10.1152/ajpendo.2001.281.5.E1063.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Body Composition / drug effects
  • Body Weight / drug effects
  • DNA / metabolism
  • Drug Resistance
  • Fatty Acids, Nonesterified / blood
  • Fatty Liver / etiology
  • Glucose / administration & dosage*
  • Human Growth Hormone / pharmacology*
  • Insulin-Like Growth Factor I / pharmacology
  • Lipid Metabolism
  • Lipids / administration & dosage*
  • Liver / drug effects*
  • Liver / growth & development*
  • Liver / metabolism
  • Parenteral Nutrition*
  • Proteins / metabolism
  • Rats

Substances

  • Fatty Acids, Nonesterified
  • Lipids
  • Proteins
  • Human Growth Hormone
  • Insulin-Like Growth Factor I
  • DNA
  • Glucose