Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer cachexia is among the most dramatic situations of depletion in body energy reserves. To ascertain whether the pattern of body composition alteration during tumour development is influenced by aging as in uncomplicated starvation, we compared the difference of body composition between Yoshida sarcoma bearing rats and young (200 g, 7 weeks) and adult (400 g, 13 weeks) control rats. After the same duration of tumour bearing, mass and composition of tumours were similar in adult and young rats, indicating that they are independent of host age. Food intake decreased to a remarkably similar value in both young and adults. Body water content was elevated in hosts of both ages. The relative deficit of body lipid vs controls was similar for both, the absolute lipid deficit being therefore larger in adult than in young tumour-bearing rats (14.3 +/- 4.4 g vs 6.8 +/- 0.9 g; P < 0.01). In contrast, there was a relatively larger deficit of body protein in young rats. Paradoxically, these rats still maintained a positive nitrogen balance whereas this balance was negative in adult tumour-bearing rats. In conclusion, as previously shown in uncomplicated undernutrition, the anorexia induced by Yoshida sarcoma development is still associated with some protein accretion in young rats whereas cachexia develops in adults.
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PMID:Body protein and lipid deficit in tumour-bearing rats in relation to age. 821 4

Many factors can modify nutritional status in cancer patients, including cachexia, nausea and vomiting, decreased caloric intake or oncologic treatments capable of determining malabsorption. Cachexia is a complex disease characterized not only by a poor intake of nutrients or starvation, but also by metabolic derangement. Nausea and vomiting may limit the nutrient intake and are most often the consequences of oncologic treatments or opioid chronic therapy. Decreased caloric intake is considered to be one of the major causes of malnutrition, although the causes of anorexia remain unclear. Malabsorption is generally attributed to the consequences of oncologic treatments reducing the gastrointestinal absorption. Biochemical measurements and immunological tests may be not reliable indicators of nutritional status in cancer patients. Therefore, medical history, physical examination, estimates of daily oral intake, weight changes and an appropriate consideration of the nutritional requirements according to the stage of disease must still be assessed. The therapeutic approaches should be individualized and realistic. Whenever possible, oral nutrition is the method of choice, with due consideration for specific dietary needs. Nausea and anorexia can be reduced by different kinds of drugs. A careful decision based on good clinical judgement is necessary before deciding to start either enteral or parenteral nutrition, to avoid a useless, costly and difficult treatment. In choosing the route for administration of nutrients, availability of and access to a functioning gastrointestinal tract, compliance and comfort of the patient, gastrointestinal toxicity due to chemotherapy or radiotherapy fields, different costs, duration and place of treatment should be considered rather than the different capacity of parenteral versus enteral nutrition. However, postoperative periods after massive intestinal resection often require prolonged parenteral nutrition. The benefits of parenteral nutrition are not often demonstrable in patients with bowel obstruction. Different ethical aspects are presented. Flexibility in attempting to meet the nutrition needs of each patient is probably the most useful guide.
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PMID:Nutrition in cancer patients. 877 Dec 86

As a complex syndrome, cachexia has different clinical manifestations; anorexia appears to be one of the most frequent findings, together with weight loss. Anorexia is the cause and partly the consequence of metabolic changes and of progressive undernourishment. In cancer cachexia, weight loss is associated with a marked decrease of food intake and severe alteration of body composition. Malnourished cancer patients show a marked loss of adipose tissue and protein mass with BIA evidence of decreased body cell mass and expansion of extracellular water. The mechanisms of anorexia and cachexia are still a matter of debate, but the possible involvement of cytokines in the pathogenesis of this syndrome has opened up new possibilities for its understanding and treatment. As a result of the multifactorial etiology of cancer cachexia/anorexia, therapies that stimulate appetite and promote greater food intake, coupled with factors that influence metabolism and cytokine production may be an optimal therapeutic strategy. Of particular interest appears to be the possible role played by fish oil in antagonizing the negative effects of cytokines. Future research in this field will help clinicians develop new methods to treat patients who have disease-induced starvation and wasting.
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PMID:Food intake and body composition in cancer cachexia. 885 Feb 14

Neuropeptide Y (NPY) neurones in the arcuate nucleus of the rodent hypothalamus may play a key role in responding to reductions in body energy stores with appropriate changes in energy homeostasis, namely an increase in food-seeking behaviour and hyperphagia, together with a reduction in heat production by brown adipose tissue. These adaptive responses are mimicked by the injection of NPY into the main sites of projection of the NPY neurones, and animals that are threatened by energy deficits (e.g. through starvation or insulin-deficient diabetes) show increased activity of these neurones. Genetically obese rodents also show hyperactivity of the NPY neurones, which is inappropriate to their energy needs and may contribute to their hyperphagia, reduced energy expenditure and excessive weight gain. The NPY neurones may be inhibited by insulin and leptin, which may both serve as signals of peripheral fat mass. Ultimately, characterization of the specific "feeding' receptors which mediate NPY's central effects on energy homeostasis may provide opportunities for designing drugs to manipulate and appetite and energy balance in man, notably obesity and the cachexia commonly associated with malignancy and chronic infection.
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PMID:Neuropeptide Y, the hypothalamus and the regulation of energy homeostasis. 887 Nov 82

Progressive wasting is common in many types of cancer and is one of the most important factors leading to the early death of cancer patients. Although anorexia frequently accompanies cachexia it has been difficult to establish a simple cause-and-effect relationship, and nutritional supplementation is not able to effectively reverse the process of cachexia. An increased resting energy expenditure may contribute to weight loss in some cancer patients and may explain the increased oxidation of fat. Futile energy-consuming cycles, such as the Cori cycle, may contribute to the increased energy demand. Unlike starvation, weight loss in cancer arises equally from loss of muscle and fat, and the process is characterized by an increased catabolism of skeletal muscle and a decrease in protein synthesis. Several experimental studies have suggested a role for the cytokines tumor necrosis factor alpha, interleukins-1 and -6, and interferon gamma as mediators of the process of cachexia, although conclusive data supporting a role in human disease are often lacking. Catabolic factors capable of direct breakdown of muscle and adipose tissue appear to be secreted by cachexia-inducing human tumors and may play an active role in the process of tissue degeneration. Pharmacologic intervention using antagonists to cachexia factors may be capable of reversing the wasting process.
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PMID:Cancer cachexia: metabolic alterations and clinical manifestations. 905 39

The child with a malignancy frequently will have associated cachexia with significant weight loss and malnutrition. The reasons for this are multifactorial and may be related directly to the tumor, such as increased metabolic rate, circulating peptides leading to anorexia, and decreased intake due to poor appetite or gut involvement. There appears to be other reasons involved, including increased whole body protein breakdown, increased lipolysis, and increased gluconeogenesis. Release of certain cytokines, such as tumor necrosis factor, interleukin-1, interleukin-6, and others may increase the cancer cachexia. Malnutrition in these children leads to intolerance of chemotherapy and radiotherapy as well as increased local and systemic infections. For many years, oncologists were hesitant to provide nutrition support to cancer patients for fear that tumor growth would be enhanced. Pediatric oncologists learned early that starvation plays no positive role in cancer therapy. Adjunctive nutritional support, either enterally or parenterally, supports the patient during therapy with surgery, chemotherapy, or radiation. Many studies have now shown that the nutritionally replete patient tolerates therapy better and in some pediatric malignancies may enhance survival.
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PMID:Nutritional support of the pediatric oncology patient. 943 98

Acute stresses such as trauma or endotoxemia augment GLN demand and are associated with increased release of this amino acid from skeletal muscle and lung as well as increased expression of glutamine synthetase (GS, the principal enzyme of GLN synthesis) in these tissues. Muscle GLN release is also increased during chronic catabolic states which are associated with depletion of lean body mass, such as starvation or malignancy. We hypothesized that the expression of GS in response to an acute stress would be altered in tumor-bearing rats (TBR) experiencing severe cachexia and therefore a previously heightened GLN demand. Male Fischer 344 rats were implanted with methylcholanthrene-induced fibrosarcoma tumors or underwent sham operations and pair-feeding (sham) with TBR partners. When tumor burden reached approximately 15% of carcass weight, animals received injections of either Escherichia coli lipopolysaccharide (LPS, 1 mg/kg body wt) or saline vehicle. Rats were sacrificed 8 h after injection and lung and muscle tissue were analyzed for GS mRNA and protein via Northern and Western blot techniques, respectively. LPS injection caused an equivalent 4- to 6-fold increase in lung and muscle GS mRNA in both TBR and sham rats (P < 0.01). LPS did not produce a significant increase in GS protein level in muscle tissue of either group or in lung tissue of sham rats. In contrast, endotoxin did lead to a 3.5-fold increase in GS protein levels in lung tissue of TBRs (P < 0.05). This increase in lung GS protein may signify the importance of the lung in maintaining GLN homeostasis during chronic catabolic states where muscle mass is diminished.
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PMID:Sepsis increases lung glutamine synthetase expression in the tumor-bearing host. 973 11

Severe weight loss associated with cancer continues to be a major cause of morbidity in cases of childhood malignancy. The etiology is not completely understood but is probably multifactorial, including reduced ingestion and altered metabolism of nutrients. Changes in the host metabolism of protein, fat and carbohydrate in the cancer-bearing host have been demonstrated both in animal models and in patients. Changes include increased protein turnover and loss of the normal compensatory mechanisms seen in starvation. Additionally, increased lipid breakdown results in depletion of lipid stores and changes in carbohydrate metabolism result in an energy-losing cycle. The increase in protein turnover seen in children with leukemia may be related to the tumor, the chemotherapy administered or to related conditions such as febrile neutropenia. The role of endogenous mediators of cancer cachexia has not yet been clearly elucidated, although tumor necrosis factor, interleukin I and interleukin 6 appear to be involved. Studies of energy expenditure in children with cancer have indicated that certain patients with a raised metabolic rate are at particular risk of severe weight loss. The challenge is to identify these vulnerable patients and to provide adequate nutritional support early in treatment and therefore avoid the deleterious effects of cachexia.
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PMID:Aspects of altered metabolism in children with cancer. 987 81

A simple formula (1.536 x TOBEC + 475.146 = LBM, where TOBEC is total body electrical conductivity and LBM is lean body mass) to estimate LBM in grams was developed on the basis of the total body fat data obtained by ether extraction and TOBEC in normal rabbits. The formula was also applicable to rabbits with cachexia induced by inoculation of VX2 carcinoma or by starvation. We were able to assess the losses of body fat in the rabbits with cachexia at 10-day intervals by using TOBEC.
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PMID:Body composition analysis of cachectic rabbits by total body electrical conductivity. 1005 Feb 70

Cancer anorexia/cachexia is a major clinical problem, especially in advanced cancer patients. Its pathogenesis is quite complex. Anorexia plays a central role, but cancer cachexia is more complex than pure chronic starvation. One of the key differences is the preferential mobilization of fat and the sparing of skeletal muscle in simple starvation compared with an equal mobilization of fat and skeletal muscle in cancer patients. An increase in basal energy expenditures seems to play a contributory role in many patients. Cytokines, essentially but not exclusively tumor necrosis factor alpha, play an essential role, and the syndrome can be compared with a low-grade chronic inflammatory state. As it is in most fields in medicine, prevention is more efficacious than treatment, and, to avoid the final and dramatic stages of cancer cachexia, adequate nutritional advice and support must be provided sufficiently early. Parenteral nutrition could facilitate the administration of complete doses of chemotherapy or radiotherapy, but no significant survival benefit or decrease in treatment-induced toxicity have ever been demonstrated in prospective randomized trials. The gut should always be used if at all possible. Percutaneous endoscopic gastrostomy is used increasingly in patients who cannot eat but who have functionally intact gastrointestinal tracts, especially in patients with head and neck cancer. Eight randomized, double-blind, placebo-controlled studies have demonstrated that progestational drugs can somewhat stimulate appetite, food intake, and energy level; increase weight in many patients; and often decrease nausea and vomiting severity; however, pharmacologic treatment of cancer cachexia remains disappointing, and more trials with anticytokine drugs should be conducted.
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PMID:The syndrome of anorexia-cachexia. 1041 77


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