TY - JOUR
T1 - Effect of growth hormone and protein intake on tumor growth and host cachexia
AU - Bartlett, David L.
AU - Stein, T. Peter
AU - Torosian, Michael H.
N1 - Funding Information:
CANCER CACHEXIA IS A CLINICAL syndrome of host wasting associated with progressive tumor growth. This catabolic state is associated with specific disorders in host protein, carbohydrate, lipid, and energy metabolism} "3 The host deteriorates as its tissues are eatabo-lized to provide substrates to the tumor for energy and protein synthesis. Nutritional support of the patient with cancer is controversial because the ability selectively to feed the tumor-bearing host without stimulating tumor growth has not been developed. 4, 5 Laboratory Supported 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. Accepted for publication July 25, 1994. Reprint requests: M.H. Torosian, MD, Hospital of the University of Pennsylvania, 3400 Spruce St., 4th Floor Silverstein, Philadelphia, PA 19104. Copyright 9 1995 by Mosby-Year Book, Inc. 0039-6060/95/$3.00 + 0 11/56/61253
PY - 1995/3
Y1 - 1995/3
N2 - 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.
AB - 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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U2 - 10.1016/S0039-6060(05)80199-0
DO - 10.1016/S0039-6060(05)80199-0
M3 - Article
C2 - 7878530
AN - SCOPUS:0028925351
VL - 117
SP - 260
EP - 267
JO - Surgery
JF - Surgery
SN - 0039-6060
IS - 3
ER -