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Insulin‐Like Growth Factor‐I but Not Growth Hormone Attenuates Dexamethasone‐Induced Catabolism in Parenterally Fed Rats
Author(s) -
Lo HuiChen,
Hinton Pamela S.,
Unterman Terry G.,
Ney Denise M.
Publication year - 1996
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607196020003171
Subject(s) - endocrinology , medicine , anabolism , catabolism , protein catabolism , parenteral nutrition , insulin , insulin like growth factor , dexamethasone , glucocorticoid , nitrogen balance , hormone , growth factor , chemistry , metabolism , amino acid , biochemistry , receptor , organic chemistry , nitrogen
Background: We demonstrated that recombinant human insulin‐like growth factor‐I (rhIGF‐I) or growth hormone (rhGH) produces identical body weight gain during total parenteral nutrition (TPN) in surgically‐stressed rats. Our current objective was to evaluate the relative anabolic and metabolic effects associated with administration of rhIGF‐I and/or rhGH during hypocaloric TPN in rats with dexamethasone (DEX)‐induced catabolism. Methods: Male Sprague‐Dawley rats (~270 g) given TPN and DEX were treated with IGF‐I and/or GH for 6 days. Two control groups, TPN and DEX, were included. Anabolic response was assessed by change in body protein content and nitrogen balance. Metabolic response was assessed by determination of serum concentrations of IGF‐1, IGF binding proteins (IGFBPs), insulin, glucose, triacylglycerol, glycerol, and free fatty acids. Results: Compared with GH, IGF‐I attenuated DEX‐induced loss of body protein and decreased serum concentrations of glucose, free fatty acids, glycerol, and triglycerol. Treatment with IGF‐I plus GH showed an anabolic response similar to IGF‐I alone. IGF‐I and/or GH increased serum concentrations of IGF‐I and IGFBP‐3. IGF‐I alone increased serum level of IGFBP‐5. Conclusion: Administration of IGF‐I, but not GH, attenuates DEX‐induced protein catabolism in association with increased insulin sensitivity in rats. Glucocorticoid excess may limit the response to GH therapy during TPN. (Journal of Parenteral and Enteral Nutrition 20: 171–177, 1996)