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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Twenty-two patients with anorexia nervosa were studied at 2-week intervals during treatment on psychiatric wards. In order to characterize the metabolic situation in starvation, levels of free fatty acids, beta-hydroxybutyric acid, and acetoacetate were measured. The endocrine adaptation to starvation was studied by measuring triiodothyronine, noradrenaline, and cortisol. Anorectic symptoms were assessed by the Anorexia Nervosa Inventory Scale (ANIS) and mood changes on the basis of a "Befindlichkeits" Scale (BF). Only half of the patients showed metabolic and endocrine signs of starvation on admission to the hospital, despite low body weight. This group had significantly more severe anorectic symptoms (ANIS) and gained weight at a lesser rate. Metabolic signs of starvation disappeared during the first 4 weeks of therapy in most of the patients. The endocrine indicators for starvation normalized much more slowly, with noradrenaline having the slowest pace. "Bulimics" and "restricters" could not be distinguished from one another by metabolic or endocrine observations. The "bulimics," however, showed more severe anorectic symptoms (ANIS) and a more depressed mood.
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PMID:Anorectic behavior, mood, and metabolic and endocrine adaptation to starvation in anorexia nervosa during inpatient treatment. 402 3

The effects of lantana poisoning on the microbial populations of the rumen and on fermentation within the rumen were compared to the effects of starvation in sheep. The protozoal and bacterial populations of the rumen were decreased to the same extent by lantana poisoning and starvation. Fermentation appeared to continue for several days in the rumen of lantana-poisoned animals, as shown by the concentrations of volatile fatty acids and ammonia, and the pH and rH of rumen fluid. It is suggested that this was due to retention of plant material in the static rumen of lantana-poisoned animals. It is concluded that lantana toxins do not affect rumen microorganisms directly and that the changes observed in lantana-poisoned animals are probably due to anorexia and rumen stasis.
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PMID:Changes in rumen contents associated with lantana poisoning of sheep. 613 5

The importance of decreased food intake as the mechanism behind altered protein metabolism in skeletal muscle in cancer was evaluated. A methylcholanthrene-induced sarcoma (MCG 101) transplanted in weight-stable and nongrowing mice (C57BL/6J) was used as the tumor-animal model. Three study groups with appropriate control groups were used: sarcoma-bearing mice; pair-fed mice; and starved mice. The synthesis of myofibrillar and sarcoplasmic proteins was decreased in sarcoma-bearing mice. This was correlated to decreased content of RNA in the muscles and caused a net loss of muscle tissue was measured by dry weight of skeletal muscles. The incorporation rate of amino acids into myofibrillar and sarcoplasmic proteins was decreased to the same extent in the pair-fed mice as that in the sarcoma-bearing mice. This probably reflected decreased protein synthesis, since the radioactivity (dpm/mg) did not differ significantly in the crude transfer RNA fraction between the groups. Separation of soluble proteins from muscle tissue by means of ion-exchange chromatography showed that the pattern of decreased protein synthesis was not tumor specific when compared to muscle affected by starvation. The decrease in protein synthesis was more or less selective, since the synthesis of basic proteins was considerably decreased and was influenced more than were neutral and acidic proteins in both cancer and starvation. Anorexia of a tumor-bearing host is a sufficient trigger to induce decreased protein synthesis in skeletal muscles, but other factors may also be of quantitative importance.
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PMID:Evaluation of anorexia as the cause of altered protein synthesis in skeletal muscles from nongrowing mice with sarcoma. 616 32

The many causes of clinical magnesium deficiency can be placed into 2 categories: diminished intake of magnesium, and enhanced losses of magnesium, either through the gastrointestinal tract or through the kidneys. Examples of the first category include alcoholism, starvation, anorexia due to neoplastic disease and/or chemotherapy. Examples of the second category include severe diarrhoeal states, gastrointestinal fistulae, malabsorption, diuretic therapy and gentamicin therapy. Estimates of the prevalence of clinical hypomagnesaemia range from 6 to 11% in hospitalised patients. Serum predictors of associated clinical magnesium depletion include hypokalaemia (42%), hyponatraemia (23%), hypophosphataemia (22%) and hypocalcaemia (20%). Experimental and clinical observations strongly support the view that magnesium and potassium are closely linked at the cellular level. Magnesium has been demonstrated to be important in cell energetics (Mg++-activated ATPase), in maintenance of the integrity of cell membranes, retardation of cell loss of potassium, as well as enhancing repletion of cell potassium. While translation of these experimental observations into clinical terms encompasses a wide spectrum of illnesses, there is special relevance in considering the role of magnesium in repletion and maintenance of cell potassium in 2 clinical instances: (a) patients treated with digitalis and diuretics; and (b) hypertensive patients. In these types of patients not only potassium but also magnesium should be administered together to avoid the problem of cell potassium depletion and refractory potassium repletion associated with coexisting and uncorrected magnesium depletion.
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PMID:Magnesium deficiency. Causes and clinical implications. 649 96

Anorexia nervosa or self-starvation is a disease that can lead to life-long problems or death. A problem primarily affecting young women, anorexia is occurring at a rapidly increasing rate in the United States. In today's society, thinness is perpetuated in all aspects of life; the result of this initial dieting in combination with a low self-concept and self-esteem appear to be factors related to this disease. This article defines anorexia nervosa, explains physical and psychological problems resulting from the disease and emphasizes the role health professionals have in the prevention and early recognition of anorexia nervosa in the adolescent.
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PMID:Anorexia and the adolescent. 655 94

This study was designed to ascertain whether the overall availability of whole-body lipids and nitrogen is a limiting factor for survival in tumor-bearing mice suffering from anorexia and cachexia. Three-month-old nongrowing mice (C57BL/6J) were given s.c. transplants of a methylcholanthrene-induced sarcoma. Freely fed, starved, and pair-fed animals were used. Body and lipid composition, tumor growth, and survival time were measured. Freely fed sarcoma-bearing mice died with profoundly altered body composition. This was not explained by the anorexia assessed in pair-feeding experiments. Starvation had caused a more severe depletion in body composition in both tumor-bearing and nontumor-bearing animals than the tumor alone did in freely fed tumor-bearing mice. Freely fed tumor-bearing animals had normal proportions of whole-body triglycerides, cholesterol, and polar lipids, but they lost palmitic acid quantitatively more than any other fatty acid. It is unlikely that any single fatty acid became limiting during tumor growth. The results show that the overall availability of lipids, nitrogen, and glucose precursors is not a limiting factor for survival in experimental tumor cachexia. Other factors considered to be more likely as determining factors for the death of tumor-bearing animals are discussed.
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PMID:Role of whole-body lipids and nitrogen as limiting factors for survival in tumor-bearing mice with anorexia and cachexia. 657 17

Protein degradation was measured as tyrosine release rate from proteins of extensor digitorum longus (EDL) muscles and as urinary excretion of 3-methylhistidine in freely fed adult nongrowing C57BL/6J mice with sarcomas, to study protein degradation in cancer-induced wasting of skeletal muscles. Whole muscle protein breakdown rate was unchanged, whereas protein synthesis was depressed, leading to an increased net degradation of skeletal muscles with loss of soluble, myofibrillar, and collagen proteins. Starvation for 24 hours elevated whole muscle protein breakdown in mice with and without sarcomas. Subsequent refeeding for 24 hours normalized the degradation. Adaptation to anorexia in pair-fed controls was achieved by a decrease in muscle protein turnover evaluated by urinary excretion of 3-methylhistidine over 5 days. The measurement of "catabolic decrease" of muscle protein breakdown protected the muscle mass in mice without tumors, but it was ineffective in tumor-bearing animals. The unchanged rate of breakdown of proteins in whole EDL muscles from tumor-bearing mice was accompanied by increased maximum cathepsin D activity and by elevated autolytic activity at acid pH in some muscles. Therefore, cathepsin D activity and net protease activities did not reflect whole muscle protein degradation in tumor-induced malnutrition. The results demonstrate that wasting of skeletal muscles in experimental cancer was not dependent on increased degradation but was dependent on depressed protein synthesis.
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PMID:Lack of evidence for elevated breakdown rate of skeletal muscles in weight-losing, tumor-bearing mice. 657 91

The effect of poisoning by the plant Lantana camara L. on reticulo-ruminal motility was investigated in sheep. There was a marked decrease in forestomach motility 4-6 h after dosing with the plant and motility continued to be depressed throughout the course of the disease. The effect of lantana on motility was characterized by a decrease in the number and median amplitude of forestomach movements. This was in contrast to the effect of starvation which caused a decrease in only the number of forestomach movements and even this effect was less severe than in lantana-poisoned animals. The effects of lantana on the components of the reflex which controls rumen motility were examined. No evidence was found for a direct effect of lantana toxins on the stretch and tactile receptors in the reticulum; on the vagus nerves; on the gastric centre or on the muscle of the forestomach. However, evidence was found to support an hypothesis that stasis of the rumen in lantana poisoning is due to inhibitory influences arising from the damaged liver. The evidence included a correlation between the onset of ruminal stasis and liver injury; a relationship between the severity of liver injury and ruminal stasis and the finding that denervation of the liver converted the pattern of forestomach movements in intoxicated animals to that seen in starved animals. It is concluded that stasis of the rumen in lantana-poisoned animals is due at least initially, to inhibitory neural impulses arising from the damaged liver and to the effects of anorexia.
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PMID:The mechanism of ruminal stasis in lantana-poisoned sheep. 668 7

The sites at which TRH produces suppression on feeding and drinking were examined anatomically in the rat brain. This was accomplished by microinjecting nmol concentration of TRH into 6 different brain sites. Intracerebroventricular injection of TRH (25, 50, 100 nmol/rat) suppressed starvation-induced feeding and drinking in a dose related manner. The microinjection in a small amount of TRH (8 nmol/hemisphere) into the medial and lateral hypothalamus produced relatively severe anorexia and adipsia as compared with the other areas including the nucleus accumbens, the substantia nigra, the globus pallidus and the amygdala. It was concluded that the medial hypothalamus is the most sensitive site of TRH-induced anorexia and adipsia and the action of TRH on the lateral hypothalamus is also a possible mechanism mediating the decrease in water intake.
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PMID:Intracranial injection of thyrotropin releasing hormone (TRH) suppresses starvation-induced feeding and drinking in rats. 681 81


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