## Abstract This study evaluated the effects of basic fibroblast growth factor, transforming growth factor‐β1, insulin‐like growth factor‐1, and insulin on the incorporation of thymidine and sulfate in human osteoarthritic articular cartilage. Tissue explants were obtained from 11 patients undergoi
Effect of insulin-like growth factor 1 on host response to tumor
✍ Scribed by Yuan-Lin Dong; R. Y. Declan Fleming; K. Fon Huang; David N. Herndon; Tina Z. Yan; Dr. J. Paul Waymack
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 579 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0022-4790
No coin nor oath required. For personal study only.
✦ Synopsis
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 Fm/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 3 1.37 k 4.3 g of tumor free body mass during the study period. The insulin treated group lost 26.34 2 7.42 g and the IGF-I group lost 5.07 ? 3.25 g ( 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-I 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.
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