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Effect of insulin‐like growth factor 1 on host response to tumor
Author(s) -
Dong YuanLin,
Fleming R. Y. Declan,
Huang K. Fon,
Herndon David N.,
Yan Tina Z.,
Waymack J. Paul
Publication year - 1993
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930530215
Subject(s) - insulin , medicine , endocrinology , growth factor , insulin like growth factor , anabolism , ketone bodies , placebo , metabolism , pathology , receptor , alternative medicine
Oncology patients suffer multiple detrimental metabolic alterations. Among these are catabolism of tumor free body mass to supply nutrients to feed the tumor. This results not only in enhanced tumor growth but also poor wound healing and immunosuppression of the tumor host. Efforts are therefore being directed at finding methods for improving the nutritional status of the tumor host without enhancing tumor growth. We investigated the ability of two hormones, insulin‐like growth factor‐1 (IGF‐1) and insulin, to improve physiologic function in tumor‐bearing animals. Tumor‐bearing animals received a continuous infusion of IGF‐1 (2.20 mg/kg/ day), insulin (820 μm/kg/day) or placebo via an osmotic minipump for 7 days. All animals were pair fed to eliminate nutritional intake as a variable. The placebo group lost 31.37 ± 4.3 g of tumor free body mass during the study period. The insulin treated group lost 26.34 ± 7.42 g and the IGF‐1 group lost 5.07 ± 3.25g ( P < 0.001, ANOVA). IGF‐1 treatment failed to alter plasma glucose, lactate, or total amino acid concentration and failed to alter hepatic ketone body concentrations, but did improve hepatic mitochondria redox potential. Finally, IGF‐1 improved splenic weight by 110% and splenic lymphocyte count by 300%. In conclusion IGF‐1 appears to offer potential in supporting tumor free host body mass without stimulating tumor growth. © 1993 Wiley‐Liss, Inc.