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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LTW(m) Leydig cell tumors were removed from Wistar Furth rats after the animals had developed anorexia and strong aversions to a novel diet consumed during tumor growth. Previous studies had reported recovery from anorexia within 24-48 hr of tumor excision but had not measured diet preference to find out if food aversions persisted beyond recovery. In the present study, which allowed the rats to choose freely between the aversive diet and a nonaversive diet for several weeks, aversions persisted from four to 25+ days. No signs of anorexia were evident during this testing phase, which followed 10 days of post-operative recuperation in which the rats were restricted to a diet of familiar laboratory chew. These results are consistent with the hypothesis that certain anorexigenic tumors, such as the LTW(m), can substantially affect food selection long after their direct effects on appetite have dissipated.
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PMID:Tumor-induced diet aversions persist after successful excision of an anorexigenic tumor. 347 26

Plasma levels of growth hormone (GH) and the effect of GH treatment have been evaluated in adult nongrowing sarcoma-bearing mice (C57BL/6J). Prepubertal tumor-bearing mice, tumor-bearing hypophysectomized Sprague-Dawley rats, and malnourished non-tumor-bearing animals served as additional groups of study and control animals. Adult sarcoma-bearing mice showed an increase in plasma levels of GH early following tumor implantation. GH levels increased further with tumor progression. The anorexia and the state of malnutrition in sarcoma-bearing mice were the major factors behind increased GH levels. Muscle wasting and body composition in the tumor-bearing host were not improved by GH treatment at doses that increased growth rate in normal growing mice with intact pituitaries or partially normalized growth rate in hypophysectomized rats. Exogenous GH supported tumor growth and host body growth to the same extent in hypophysectomized rats. Exogenous GH in excess of endogenous GH did not stimulate tumor growth further. It is suggested that increased GH production in a tumor-bearing host acts in concert with other hormones to stimulate endogenous substrate mobilization and in tumor-bearing animals to prevent substrate deficiency and hypoglycemia. On the basis of this conclusion, it is unlikely that GH supplementation to a freely eating tumor-bearing host will support replenishment of host tissues.
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PMID:Growth hormone and experimental cancer cachexia. 348 Mar 85

In F344 rats bearing transplantable 3-methylcholanthrene (CAS: 56-49-5)-induced sarcomas, plasma concentrations of immunoreactive insulin were decreased following the development of mild or severe anorexia. Plasma levels of immunoreactive glucagon and lactate were elevated in severely anorectic tumor-bearing (TB) rats, while plasma glucose concentrations remained normal. Both groups of TB rats exhibited decreased plasma levels of serine, glutamine, citrulline, and tryptophan and increased concentrations of alanine. Plasma levels of proline and phenylalanine were also elevated in the severely anorectic TB rats. In a second experiment, 7 daily treatments with insulin corrected the anorexia for 6 days and increased body weights of TB rats. Plasma concentrations of lactate and immunoreactive glucagon were decreased, and the abnormal plasma concentrations of glutamine, proline, analine, and phenylalanine were altered toward normal following the insulin treatments. Therefore, these data are consistent with insulin treatments benefiting the TB host by increasing feeding, increasing body weight, reducing tumor glycolysis and metabolism, reducing gluconeogenesis, and reducing host catabolism, while not stimulating tumor growth. Thus insulin therapy may have potential benefits in cancer treatment by shifting glucose metabolism toward the host and away from the tumor.
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PMID:Reversal of tumor-induced biochemical abnormalities by insulin treatment in rats. 352 58

Progressive weight loss and anorexia are frequent phenomena in cancer patients. Although cachexia is an expected occurrence in the terminal stages of nearly all malignancies, it may be a presenting sign when the tumor burden is quite small. Lipid depletion occurs out of proportion to the protein loss and accounts for most of the weight loss in cancer. Lipids, more specifically fatty acids, are the major source of fuel in mammals and may also be used in the synthesis of new cell products. Lipolysis and lipogenesis are under the influence of several important enzymes and peptide hormones that may be modulated by a variety of exogenous factors. There is evidence that cancer patients have lost the normal homeostatic responses to decreased energy intake or starvation that allow a decrease in oxygen consumption and protein sparing. An increase in Cori cycle activity or futile recycling of metabolic products occurs with a net energy expenditure rather than energy production. Clinical studies have shown that the body lipid depletion accompanying tumor progression is not solely secondary to decreased food intake and may be reproduced by the transplantation of certain noninvasive tumors to normal hosts. Elevated basal lipolysis has occasionally been seen early in tumor growth. Such findings suggest the presence of a tumor-associated factor responsible for this increase in lipid mobilization. Some of the potential mechanisms for the altered lipid metabolism seen in cancer have been discussed. Metabolic substrates may be remodeled and directed away from fuel-efficient into energy-requiring pathways. An increased energy expenditure may occur as a result of the energy costs of tumor synthesis, an uncoupling of oxidative phosphorylation, or energy-requiring futile cycling. An overall depletion of lipid may be the final outcome of the inhibition of lipid deposition. TNF/cachectin has recently been found to suppress the activity and synthesis of several key lipogenic enzymes, including lipoprotein lipase. Abnormalities in insulin secretion or sensitivity may be involved in the decrease of fat storage in malignancy. Insulin also exerts a significant antilipolytic effect by its antagonism of hormone-sensitive lipase. Mediators of lipolysis and abnormal lipid metabolism may occur in a number of clinical conditions and include ectopic hormone production, growth factors, and tumor-associated lipolytic factors (lipid mobilizing factor, toxohormone).
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PMID:Fat metabolism and cancer. 353 75

This study evaluated whether altered insulin metabolism is a key factor behind weight loss during sarcoma growth in nongrowing mice (C57BL/6J). Fasted sarcoma-bearing mice had decreased blood glucose concentrations but unchanged levels of insulin, compared with those in pair-weighed and freely fed controls. During refeeding, insulin levels were inappropriately low for the degree of glycemia in sarcoma-bearing mice compared with those of pair-weighed and freely fed controls. Injections ip of glucose to tumor-bearing animals resulted in insulin levels comparable to postabsorptive values in healthy control animals, indicating that hypoinsulinemia in freely eating tumor-bearing animals was due to a reduced glycemic sensitivity for pancreatic insulin release. Insulin supplementation at doses [4 IU/100 g (body wt)] that increase body fat in normal animals could not protect the tumor-bearing host from progressive loss of body fat or lean tissues. Exogenous insulin in excess of endogenous insulin production did not stimulate tumor growth. Nitrogen and RNA-DNA content were significantly decreased in the quadriceps muscle of tumor-bearing mice. This reduction was independent of altered insulin levels and could not be prevented by exogenous insulin. The depressed capacity of protein synthesis in extensor digitorum longus (EDL) muscle could be entirely attributed to the state of malnutrition in tumor-bearing animals. The sensitivity and responsiveness of protein synthesis in EDL muscles to insulin were normal in tumor-bearing mice, regardless of whether exogenous insulin exerted its effect in vivo or in vitro. This study confirms insulin resistance for glucose metabolism in an experimental sarcoma animal model. Such changes are concluded to be secondary to anorexia and necessary to counteract hypoglycemia. In non-growing sarcoma-bearing mice, malnutrition and anorexia account entirely for depressed muscle protein synthesis, which is not explained by insulin resistance at the translational level. Insulin metabolism is not a key factor behind progression of wasting in sarcoma-bearing mice, but anorexia is.
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PMID:Role of insulin in development of cancer cachexia in nongrowing sarcoma-bearing mice: special reference to muscle wasting. 355 91

Two closely related lines of the same Walker 256 carcinoma in Crl-CD/COBS rats, described as behaving differently as regards tumor growth and host reaction, show different chemotherapeutic sensitivity to cyclophosphamide (CPA). Line B, which induces early cachexia with marked anorexia, is only moderately sensitive to CPA, while line A, which causes mild anorexia and only terminal cachexia, shows marked responsiveness to CPA, cure being attained in 75% of animals treated with a single dose of 120 mg/kg and in 90-100% of those given 20 mg/kg every other day. Comparative studies in both tumor lines on the distribution of CPA in vivo and on its metabolism by the liver perfusion technique showed no appreciable differences between the two lines in the pharmacokinetics of the compound, but indicate a much greater metabolizing capacity of CPA in the Walker 256/A animals. In vitro metabolic and covalent binding studies confirm that the liver of the Walker 256/A group metabolizes and covalently binds twice as much CPA as the liver of the Walker 256/B group. Conversely to Walker B, microsomal preparations of the Walker tumor line A are able to metabolize CPA to intermediates which irreversibly bind to tissue macromolecules, suggesting an in situ activation of the compound in the sensitive Walker tumor.
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PMID:Different sensitivity of two Walker 256 carcinoma lines to cyclophosphamide: correlation with drug distribution, biotransformation and macromolecule binding. 372 87

Rats with experimental tumors developed strong aversions to a novel diet they consumed during tumor growth. Aversions were not evident when the food available during tumor growth was familiar laboratory chow. The impact of learned food aversions on tumor anorexia was evidenced by more severe and long-lasting hypophagia in tumor-bearing animals maintained on a novel diet than in those maintained on laboratory chow. Thus, when a diet is a salient target for the development of learned aversions, the aversions that develop to it can make substantial contributions to the overall syndrome of tumor anorexia. In addition, frequent changes of the diet offered to tumor-bearing rats was associated with milder anorexia than that produced by maintaining tumor-bearing rats on a constant diet. Apparently, the prevention of learned food aversions, or the repeated replacement of aversive foods, can minimize the impact of learned food aversions and attenuate anorexia in tumor-bearing animals.
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PMID:Tumor growth in rats: conditioned suppression of food intake and preference. 384 3

Recent research addressing possible causes of the decline in spontaneous food intake which accompanies tumor growth and antitumor therapies is reviewed. Investigations of whether disruptions in brain mechanisms involved in feeding are responsible for cancer anorexia are briefly summarized. Studies evaluating the contributions of learned food aversions to the anorexia induced by tumors and antitumor therapy are discussed in some detail. Evidence is presented, from both the clinic and the laboratory, that learned food aversions occur as a result of the association of foods with the discomfort induced by chemotherapy and/or tumor growth. The possible role these aversions play in the etiology of cancer anorexia is discussed, and studies aimed at developing methods for preventing them are described.
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PMID:Physiological and psychological mechanisms of cancer anorexia. 612 39

Two studies were conducted to measure the metabolic influence of tumor growth in rats. Parameters for the metabolic state were wound-healing qualities of colon and skin. Both early and later stages of tumor growth lowered wound healing qualities to a statistically significant degree. No anorexia or weight loss was found in this rat-tumor model during the study period. Intravenous hyperalimentation (IVH; with proteins and carbohydrates) of tumor-bearing rats stimulates tumor growth but at the same time restores wound-healing qualities to control levels, both during early and later stages of tumor growth. It is suggested that tumor growth leads to an as yet not measurable disturbance of the metabolic equilibrium but that IVH can replenish the tumor-bearing host and restore the metabolic equilibrium.
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PMID:The influence of intravenous hyperalimentation (IVH) on wound healing in tumor-bearing rats. 641 78

The independent effects of total parenteral nutrition (TPN) on tumor growth and host carcass are important in designing effective nutritional support. In this study, a TPN regimen was used to keep substrate intake at normal levels during a 10-day period of tumor-induced anorexia and cachexia in rats transplanted with a sarcoma. Tumor mass was increased in TPN-supported animals compared to orally-fed controls. Tumor composition (water, fat, nitrogen) was similar in all tumors. Host carcass mass in tumor-bearing (TB) animals was increased by TPN as compared to orally-fed TB controls, but not to the same extent as in orally-fed or TPN-supported nontumor-bearing controls. Host carcass composition determinations demonstrated significantly increased fat content but no significant change in protein or water content in TB-TPN animals compared to orally-fed TB animals. This study demonstrates increased tumor growth and increased host carcass fat stores secondary to TPN.
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PMID:Tumor and host carcass changes during total parenteral nutrition in an anorectic rat-tumor system. 642 Dec 54


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