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)

A delayed wasting syndrome similar to that induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was observed in male Sprague-Dawley rats exposed to 3,3', 4,4'-tetrachloroazoxybenzene (TCAOB) and 3,3',4,4'-tetrachloroazobenzene (TCAB). After a slow growth period, all treatment animals (25 mg/kg, i.p., 2 doses per week) exhibited a starvation-like syndrome characterized by reduced food intake, dramatic loss of body weight and subsequent death. Although the growth of all major organs in the treatment animals was affected, the thymus appeared severely atrophied. The growth kinetics during the earlier phase were further analyzed using serially-killed rats receiving TCAOB. In addition, TCAOB was found to markedly depress the specific activity (mumol/min/g wet liver) of glucose-6-phosphatase, fructose-1,6-bisphosphatase, phosphoenolpyruvate carboxykinase, and pyruvate kinase in the liver. Significant changes in the levels of cytochrome P-450, glutamic-pyruvic transaminase and malic enzyme in the liver were also observed.
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PMID:Delayed wasting syndrome and alterations of liver gluconeogenic enzymes in rats exposed to the TCDD congener 3,3', 4,4'-tetrachloroazoxybenzene. 401 2

The progressive nutritional deterioration frequently found in cancer patients, is often referred to as cancer cachexia. In contrast to starvation, where it is possible to reverse the body composition changes by the provision of extra calories, in cancer cachexia this reversal is not observed, suggesting that anorexia alone is unlikely to be responsible for this wasting syndrome. Over the past decades a number of studies have focused on the possible mediators which may be responsible for metabolic abnormalities observed in cancer patients. Pro-inflammatory cytokines have been strongly implicated, but evidence supporting such a direct role is lacking. Recently, exciting work regarding molecules produced by tumour cells, and which may induce lipolysis and proteolysis, has been published. There is also evidence that increased metabolism of host resources may provide substrates which might promote tumour growth. A number of studies have demonstrated that polyunsaturated fatty acids, such as linoleic and arachidonic acid, are able to promote tumour cell growth either by directly stimulating mitosis or by inhibiting apoptosis. Even more interesting is the discovery of antagonists of these catabolic factors such as eicosapentanoic acid for the lipolytic factor, which may play a role in the treatment of these patients in the near future.
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PMID:Metabolic responses to tumour disease and progression: tumour-host interaction. 1110 99

Approximately two thirds of cancer patients at advanced stages of the disease suffer from anorexia, which leads to significant weight loss and progressive cachexia, an important factor that contributes to death. It has been observed that cancer cachexia differs from simple starvation, although the exact mechanisms associated with cancer cachexia are not well known. Several theories regarding its pathogenesis point to a complex mixture of tumor, host and treatment variables. Unfortunately, the wasting syndrome also constitutes for the patient, a progression of the cancer process, significantly affecting quality of life and social interactions. Treatable causes should be identified and treated. Knowledge of the mechanisms underlying the effects of caquexia on the patient may play a role in identifying treatment measures targetted to muscle wasting and to maintain body strength. In this article we review the main features and mechanisms of the anorexia-cachexia syndrome in patients with cancer.
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PMID:[The cachexia-anorexia syndrome among oncological patients]. 1904 64

Cancer anorexia-cachexia syndrome (CACS) is a lethal but poorly defined involuntary wasting disorder. Loss of skeletal muscle and fat distinguishes it from starvation. Cachexia has been described as a clinical syndrome since ancient times, and the poor prognosis has long been acknowledged. In this article we have reviewed historical perspectives on cancer cachexia, and commented on modern definitions. In cancer cachexia, most historical descriptions included anorexia, wasting and a pale complexion. Other associated symptoms, such as fatigue, early satiety and taste changes, were inconsistently described. Newer descriptions have not significantly expanded the clinical picture.Today, there is still no consensus definition, hindering research on early diagnosis and effective therapy. The language descriptors used to characterise the syndrome are important. For example, the word 'cachexia' itself may mislead; perhaps cancer-related wasting syndrome is more accurate. Cancer anorexia-cachexia syndrome is a disorder associated with high morbidity and mortality, and deserves greater attention in both clinical and translational research.
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PMID:What is cancer anorexia-cachexia syndrome? A historical perspective. 2060 45

The hypothalamus-pituitary-thyroid feedback control is a dynamic, adaptive system. In situations of illness and deprivation of energy representing type 1 allostasis, the stress response operates to alter both its set point and peripheral transfer parameters. In contrast, type 2 allostatic load, typically effective in psychosocial stress, pregnancy, metabolic syndrome, and adaptation to cold, produces a nearly opposite phenotype of predictive plasticity. The non-thyroidal illness syndrome (NTIS) or thyroid allostasis in critical illness, tumors, uremia, and starvation (TACITUS), commonly observed in hospitalized patients, displays a historically well-studied pattern of allostatic thyroid response. This is characterized by decreased total and free thyroid hormone concentrations and varying levels of thyroid-stimulating hormone (TSH) ranging from decreased (in severe cases) to normal or even elevated (mainly in the recovery phase) TSH concentrations. An acute versus chronic stage (wasting syndrome) of TACITUS can be discerned. The two types differ in molecular mechanisms and prognosis. The acute adaptation of thyroid hormone metabolism to critical illness may prove beneficial to the organism, whereas the far more complex molecular alterations associated with chronic illness frequently lead to allostatic overload. The latter is associated with poor outcome, independently of the underlying disease. Adaptive responses of thyroid homeostasis extend to alterations in thyroid hormone concentrations during fetal life, periods of weight gain or loss, thermoregulation, physical exercise, and psychiatric diseases. The various forms of thyroid allostasis pose serious problems in differential diagnosis of thyroid disease. This review article provides an overview of physiological mechanisms as well as major diagnostic and therapeutic implications of thyroid allostasis under a variety of developmental and straining conditions.
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PMID:Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. 2877 11