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At least 109 records · Page 6Linked to original sources
PubMed1992

Lipid metabolism in cancer cachexia.

The effect of cancer cachexia on the oxidative metabolism of lipids has been studied in mice transplanted either with the MAC16 adenocarcinoma, which induces profound loss of body weight and depletion of lipid stores, or the MAC13 adenocarcinoma, which is the same histological type, but which grows without an effect on host body weight or lipid stores. While oxidation of D-[U-14C]glucose did not differ between animals bearing tumours of either type and non-tumour bearing controls, oxidation of [1-14C]triolein administered by intragastric intubation was significantly (P less than 0.05) higher in animals bearing the MAC16 tumour than in either non tumour-bearing controls or in animals bearing the MAC13 tumour. Intestinal absorption of [14C]lipid was significantly (P less than 0.05) reduced in animals bearing the MAC13 tumour when compared with either non tumour-bearing animals or MAC16 tumour-bearing animals, but was not significantly different in the latter two groups. The level of labelled lipids in heart and adipose tissue after an oral [14C]lipid load was significantly lower in animals bearing the MAC16 tumour compared with the other two groups. The level of tumour lipids was also higher in the MAC16 than in the MAC13 tumour after both an oral [14C]lipid load or by direct injection of [U-14C]palmitate complexed to albumin into epididymal fat pads. Oxidation of [U-14C]palmitate was also significantly enhanced in liver and heart homogenates from animals bearing the MAC16 tumour. These results suggest that in cachectic tumour-bearing animals mobilisation of body lipids is accompanied by an increased utilisation.

Adenocarcinoma↗
PubMed1990

Biochemical manifestations of a rat mammary adenocarcinoma-producing cachexia: in vivo and in vitro studies.

The physical and metabolic characteristics of a Dark Agouti rat mammary adenocarcinoma and its effects on host metabolism are described. The tumour was characterized by a lack of glandular differentiation, tetraploidy, a rapid mitotic index and a high rate of glycolysis. The adenocarcinoma was readily maintained in tissue culture and could be passaged through the host by inoculating either cell suspensions or tissue explants. In the rat, tumour growth resulted in a loss of adipose tissue at a tumour mass of less than 5% body weight indicating that increased energy expenditure was already present at that stage. In addition the tumour caused anaemia, hypercalcaemia and hypoglycaemia. Hyperketonaemia was also observed in fasted tumour-bearing rats. Methotrexate arrested tumour growth in vivo. These aspects of the tumour model make it useful for investigations into host-tumour competition and mechanisms of cachexia.

Adenocarcinoma↗
PubMed1989

Diet-induced thermogenesis in patients with gastrointestinal cancer cachexia.

1. Indirect calorimetry has been used to measure resting energy expenditure (REE) and the thermogenic response to a test meal (diet-induced thermogenesis) in groups of weight-stable and weight-losing patients with gastrointestinal adenocarcinoma. Average daily intakes of energy and protein were computed from dietary assessment for the week before hospitalization. Results were compared with a control group of patients with benign gastrointestinal disease. 2. Weight-losing cancer patients had a significantly reduced mean total energy and protein intake. 3. There was no significant difference in REE between the groups when results were normalized in terms of metabolic body size (kJ/kg 0.75) and lean body mass (kJ/kg). 4. Diet-induced thermogenesis was reduced in weight-losing cancer patients. 5. It is suggested that the reduction of diet-induced thermogenesis in weight-losing cancer patients is another element of starvation adaptation, subsequent to their weight loss, and that altered thermogenesis does not contribute to the weight loss seen in cancer cachexia.

Adenocarcinoma↗
PubMed1979

[Diabetic neuropathic cachexia (author's transl)].

Marked weight loss with cachexia together with severe depression and pain from symmetrical peripheral neuropathy were noted in a 66-year-old man, known to have had diabetes for six years, which required insulin on admission to hospital. The patient died of bronchopneumonia after one year. The severe neuropathy was proven both neurophysiologically and at necropsy. There was no diabetic retinopathy and no histological evidence of renal glomerulosclerosis. There was no evidence of a malignant tumour either clinically or at necropsy.

Aged↗
PubMed1991

Long-term inhibition of tumor growth by tumor necrosis factor in the absence of cachexia or T-cell immunity.

The relationship between detrimental (cachectic) and beneficial (antitumor) effects of tumor necrosis factor (TNF) was studied in mice bearing murine tumors transfected to secrete human TNF. In vitro, the TNF-producing transfectants were resistant to the secreted TNF and grew at rates similar to those of untransfected cells or transfected cells that did not secrete TNF. However, tumors formed by the TNF-secreting cells in vivo remained much smaller than the nonsecreting (transfected and untransfected) tumors. This inhibition of tumor growth required only relatively low serum levels of TNF, persisted for many weeks, and was independent of T cells since it occurred in nude mice. Growth of the TNF-secreting tumors increased dramatically after treatment with anti-human TNF antibody, indicating that extracellular TNF secreted by the tumor cells was necessary for the tumor inhibition. Severe weight loss characteristic of cachexia only occurred in animals with very high serum TNF levels (250 pg/ml) and could be prevented or reversed by anti-TNF antibody treatment. These data are consistent with the existence of a therapeutic window in which persistent exposure to human TNF can lead to prolonged inhibition of tumor growth in the absence of T-cell immunity or severe weight loss and without development of resistant tumor variants.

Animals↗
PubMed1985

Anorexia and weight loss: indicators of cachexia in small cell lung cancer.

A study was conducted to determine the incidence and extent to which anorexia, a decrease in spontaneous food intake, contributes to the occurrence of cancer cachexia. Data for ten male subjects with small cell carcinoma of the lung are reported for a five-month period following diagnosis. Although body weights of the subjects at the time of diagnosis averaged less than 95% of the usual weight (weight 6 months prior to diagnosis), they were greater than 109% of the mean ideal weight. At five months, the mean weight (N = 8) was 88% of the preillness weight. From the time of diagnosis, there was a mean loss of 7.2 kg (15.8 lb). The urinary creatinine excretion was below the normal range, whereas the urinary urea nitrogen values were within the normal range. At the time of diagnosis, the mean triceps skin-fold measurements were approximately 80% of the standard reference for males. During the five-month period, the mean midarm muscle circumference determinations remained greater than 90% of the reference standard. The mean serum transferrin values were 10% or more below the reported lower range of normal, whereas the great majority of the serum albumin values were 3.0 g/dl or above during the five-month period. The mean caloric intake of 2,204 kcal at the time of diagnosis was only 86% of the estimated basal energy expenditure (BEE) times a factor of 1.5 used to account for moderate activity. Four months following diagnosis, the mean caloric intake had fallen to 1,702 kcal, only 67% of the BEE X 1.5 (calculated from the weight at diagnosis). The findings provide evidence of a decline in spontaneous food intake, a small decrease in body fat, and a greater than 13% weight loss. The oral intake was less than adequate for any activity beyond the basal state. Decreased intake could account for most of the weight loss observed in the subjects.

Adult↗
PubMed1988

Cachectin: a hormone that triggers acute shock and chronic cachexia.

Septic shock and invasive infection are diseases caused by humoral mediators of both exogenous and endogenous origin. The search for and identification of these factors has led to the discovery and molecular cloning of cachectin. This pyrogenic cytokine is identical to tumor necrosis factor (TNF) and, when released into the circulation, causes profound shock and multiple organ injury. Cachectin antibodies protect against the lethal effects of mice given endotoxin and baboons given E. coli, a result suggesting that this mediator is both necessary and sufficient to provoke septic shock. Cachectin is produced in humans after endotoxin infusion; the infusion of small doses of TNF is associated with fever, rigors, headache, and hypotension. Septicemic patients also produce cachectin, and during meningococcal infection, patients with the highest serum levels of cachectin die. Chronic cachectin production causes a potentially lethal syndrome of cachexia, anemia, and protein and lipid wasting. Future investigation is being directed toward the development of cachectin antibodies for use in treating the humorally mediated systemic complications of infectious disease.

Animals↗
PubMed1988

Tumor necrosis factor not detectable in patients with clinical cancer cachexia.

Tumor necrosis factor (TNF) has been implicated in the pathogenesis of cachexia in neoplastic and infectious diseases. To assess the relationship between TNF and weight loss among cancer patients, we assayed TNF levels in serum from 19 patients who had lost 8%-40% of premorbid weight. The weight loss experienced by these patients was not attributable to anticancer therapy, gastrointestinal disorders, or other medical problems. TNF was measured using a quantitative sandwich enzyme-linked immunosorbent assay that is sensitive to human TNF in serum at concentrations greater than or equal to 40 pg/mL. No TNF was detected in serum samples from the 19 patients studied.

Adult↗
PubMed1988

Cancer cachexia.

Despite recent advances in the delivery of nutritional support, cachexia continues to contribute to the morbidity and mortality of cancer patients. This impasse has called for a review of the many factors that are believed to be associated with weight loss in the cancer host. This article reviews the topic with a view to past problems and areas for investigation in the future.

Cachexia↗
PubMed1987

Interleukin 1, tumour necrosis factor-alpha (cachectin) and the pathogenesis of cancer cachexia.

Soluble proteins synthesized and released by phagocytic cells may be responsible for the protein and energy wasting frequently observed during catabolic states, including cancer cachexia. This hypothesis is based upon the observation that many of the hosts's metabolic responses to infection, inflammation, accidental trauma and some forms of cancer are remarkably similar. Anorexia and degradation of skeletal and connective tissue protein, as well as increases in hepatic protein synthesis and energy expenditure, can all be reproduced by the administration of activated macrophage products. During inflammatory states, including active tumour growth, increased production of some cytokines, including interleukin 1 and tumour necrosis factor-alpha (cachectin), have been observed. If these monokines serve as metabolic inducers, then efforts to block therapeutically the actions of macrophage-secreted substances may play a role in slowing the progression of tissue-wasting associated with catabolic states, particularly due to malignant tumours.

Animals↗
PubMed1991

Cachexia and tumour necrosis factor-alpha in cytomegalovirus infection.

Although cachexia is a common feature of cytomegalovirus infection, little is known about its cause. To explore any contributory role that tumour necrosis factor-alpha (TNF) might have the serum concentrations of TNF in eight patients who developed CMV disease after liver transplantation were investigated. All patients exhibited pronounced and long lasting increases in TNF serum concentrations. Increased endogenous TNF concentrations were associated with weight loss and anorexia. In contrast, liver transplant recipients without CMV disease showed no weight loss.

Cachexia↗
PubMed1992

Insulin-like growth factor I preserves host lean tissue mass in cancer cachexia.

Insulin-like growth factor I (IGF-I) has been implicated in the regulation and maintenance of skeletal muscle protein balance and thus may be of potential benefit in attenuating the cancer-cachectic process. To examine this hypothesis, 47 sham or tumor-implanted Fischer 344 rats were randomized to receive either continuous subcutaneous IGF-I (220 or 400 micrograms/day) or saline as control. In the tumor-bearing (TB) population, IGF-I-treated groups showed a dose-dependent increase in host weight gain (P less than 0.05), final carcass weight (P less than 0.05), and gastrocnemius muscle weights (P less than 0.05) and protein contents (0.50 +/- 0.02, 0.40 +/- 0.01, and 0.52 +/- 0.03 g/100 g host wt, for non-TB saline, TB saline, and TB 400 mg IGF-I groups, respectively; P less than 0.01, IGF-I vs. saline). Similar increases in muscle RNA and DNA contents (P less than 0.01) were induced by IGF-I treatment (P less than 0.05). IGF-I treatment in this rat sarcoma model significantly reduced the proportion of aneuploid cells in the tumor (aneuploid-to-diploid ratio: TB saline 1.1 +/- 0.2 vs. TB IGF-I 0.5 +/- 0.1; P less than 0.05). IGF-I treatment attenuated host muscle protein and lean tissue depletion without stimulation of tumor growth. The tumor aneuploid population was reduced in response to IGF-I treatment. Thus IGF-I may be a potential therapeutic agent in cancer-induced cachexia.

Analysis of Variance↗
PubMed1990

Metabolic response to enteral food in different phases of cancer cachexia in rats.

The resting energy expenditure (REE) and postprandial energy expenditure (PPEE) were measured using closed-circuit indirect calorimetry in Walker 256 carcinosarcoma-bearing rats. The results were compared to the appropriate controls. The PPEE measurements were performed after oral test feeding. At the beginning of the tumor growth, the REE and PPEE were similar in all groups. In the second week, the tumor-bearing rats showed increased REE and decreased PPEE. The tumor-bearing rats lost weight and became anorectic. After day 14, the REE rapidly dropped to very low values and the body weight continued to decrease. This study makes it possible to differentiate three phases of cancer cachexia: silent or preclinical, hypermetabolic and hypometabolic.

Animals↗
PubMed1992

Megestrol acetate for anorexia and cachexia.

Based on promising preliminary information obtained from uncontrolled pilot studies, several randomized, placebo-controlled, double-blind clinical trials have been launched to evaluate the effectiveness of megestrol acetate for the treatment of patients with anorexia and/or cachexia. The results of these studies have demonstrated that megestrol acetate can improve patients' appetites and promote nonfluid weight gain in some. They also suggest that megestrol acetate has antiemetic properties. Ongoing clinical trials are evaluating the dose-response relationship of megestrol acetate for these clinical problems and whether megestrol acetate will improve the survival of patients at risk for developing cancer anorexia/cachexia.

Anorexia↗
PubMedDate not supplied

Influence of total parenteral nutrition on tumor growth and polyamine biosynthesis of fibrosarcoma-bearing rats after induced cachexia.

The effect of a protein-free diet (PF) or a restricted intake of chow (RI) and subsequent host repletion with total parenteral nutrition (PF-TPN, RI-TPN) on tumor growth and polyamine metabolism of fibrosarcoma-bearing rats was examined. Host weight was significantly reduced by PF and RI. Tumor growth was reduced in malnourished rats with the PF regimen resulting in the greatest decrease. Rats receiving TPN after 14 days of the RI or PF regimens had higher host weight and plasma albumin levels than malnourished rats. Tumor growth during TPN was evaluated as the percent increase and compared with that of the respective malnourished rats. The percent increase for RI-TPN rats was significantly greater although a trend toward an increase was also evident for PF-TPN rats. Tumor ornithine decarboxylase (ODC) activity and putrescine levels were increased for PF rats and decreased for RI rats while tumor ODC activity was consistently increased by TPN. Tumor growth, ODC activity, and putrescine levels were simultaneously increased only for those rats fed the RI regimen prior to TPN. These results show a disparity in tumor ODC activity, putrescine levels, and tumor growth in malnourished rats. The results of this study suggest that the nutritional origin of cachexia influences the response of the tumor to TPN and emphasizes the importance of considering the methods to induce malnutrition in designing therapuetic regimens.

Animals↗
PubMed1991

Chinese hamster ovarian cells transfected with the murine interleukin-6 gene cause hypercalcemia as well as cachexia, leukocytosis and thrombocytosis in tumor-bearing nude mice.

The effects of interleukin-6 (IL-6) in vivo were assessed by inoculating Chinese hamster ovarian (CHO) cells which were transfected with the murine IL-6 gene in nude mice. Nude mice bearing CHO cells expressing IL-6 developed hypercalcemia. Tumor-bearing mice also showed increases in white cell count, platelet count, and decreases in body weight. In nude mice carrying CHO tumors which had not been transfected with the IL-6 gene, there were no changes in these parameters. These results suggest that increased circulating concentrations of IL-6 in patients with malignant disease may contribute to a number of paraneoplastic syndromes including hypercalcemia, cachexia, leukocytosis and thrombocytosis.

Animals↗
PubMed1975

Lateral hypothalamic demyelination and cachexia in a case of "malignant" multiple sclerosis.

A 41-year old woman had profound weight loss and cachexia as a manifestation of rapidly fatal multiple sclerosis. Demyelinating lesions were present in the lateral hypothalamus. Data from animal experiments have indicated that lateral hypothalamic lesions cause a weight loss associated with a lowering of the regulation level or "set-point" for body weight. This case suggests, therefore, that a rapid decline in the level of maintained body weight in a patient without pituitary disease or general organic disorder, or distinct emotional disorder, may represent a clinical manifestation of tissue injury of the lateral hypothalamus.

Adult↗