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Background. Growth hormone supplementation has been shown to stimulate muscle protein synthesis
and to improve nitrogen balance in a variety of catabolic states. The role of growth
hormone to support the tumor-bearing host is complicated by the risk that growth hormone
or its intermediaries may stimulate tumor growth. The purpose of this study is to
examine the effect of growth hormone supplementation in tumor-bearing rats. This is
studied in the protein-fed and protein-starved state in an attempt to isolate a selective
benefit for the host over the tumor.
Methods. Forty Lewis rats bearing a metastatic mammary adenocarcinoma (MAC-33) were divided
into four groups: one receiving a regular diet plus saline solution, one receiving
a regular diet plus growth hormone (1 IU/kg/day), one receiving protein-depleted diet
plus saline solution, and one receiving a protein-depleted diet plus growth hormone.
After 25 days of growth hormone treatment, animals were killed to determine primary
tumor size, tumor/carcass ratio, host organ composition, pulmonary metastasis, and
serum amino acid levels.
Results. The tumor/carcass ratio was decreased as a result of growth hormone treatment in
both the protein-fed and protein-starved groups. Growth hormone supplementation resulted
in increased carcass weight, muscle weight, and muscle protein content in the protein-fed,
tumor-bearing animals (p<0.05). In the protein-starved, tumor-bearing rats growth hormone supplementation
resulted in a significant decrease in tumor volume and tumor protein content. Amino
acid analysis suggests that the amino acid tyrosine is a rate-limiting substrate for
tumor cell proliferation in this model.
Conclusions. Growth hormone has a differential effect on tumor and host growth in the protein-fed
and protein-starved state. Growth hormone supplementation inhibited tumor growth in
protein-deprived animals. This is most likely accomplished indirectly by limiting
amino acid substrate availability to the tumor.
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Article info
Publication history
Accepted:
July 25,
1994
Footnotes
1Supported in part by a Faculty Fellowship grant (T86-00279-011) from the Pew National Nutrition Program and American Cancer Society Career Development Award 87-114.
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© 1995 Mosby-Year Book, Inc. Published by Elsevier Inc.
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