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)

Performance characteristics of the central nervous, cardiovascular, respiratory and muscular systems in man postoperatively have received little investigative attention, despite the well known syndrome of postoperative fatigue. The impairmen in perception and psychomotor skills that has been shown to result from caloric restriction, bedrest, sedation and sleep deprivation suggests that a similar deficit may occur after surgical procedures. After a simple elective surgical procedure, maximal oxygen uptake decreases and the adaptability of heart rate to submaximal workloads is impaired. Similar deleterious effects on cardiorespiratory performance have been documented with starvation and bedrest; an understanding of cardiorespiratory performance postoperatively awaits further investigation. Maximal muscular force of contraction is also impaired by caloric restriction and bedrest, suggesting that similar effects may be seen in the postoperative state, although this has not been studied. A better understanding of the syndrome of postoperative fatigue could be achieved by a descriptive analysis of physiologic performance postoperatively. Such descriptive data could form the basis for objective evaluation of therapeutic measures intended to improve performance, such as nutritional supplementation and pharmacologic intervention. The observation that exercise with the patient in the supine position may decrease the impairment in maximal aerobic power otherwise expected in immobilized patients suggests that controlled exercise therapy may be of value in reducing physiologic impairment postoperatively.
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PMID:Understanding postoperative fatigue. 35 38

By presenting the salient aspects of a case study of a high school student athlete, we have attempted to show how participation in sports can negatively impact on self-concept, self-esteem, physical acceptance, and self-efficacy, thereby contributing to an overall feeling of inadequacy, helplessness, hopelessness, and ultimately leading to depression and chronic fatigue. An early maturer, this student experienced early success in several sports without a great deal of effort and investment, and derived much of his sense of being from the recognition and reinforcement accorded him by significant others, most notably from a father who placed a higher premium on success in athletics than on other equally worthwhile pursuits. When continued success was not forthcoming, and as later-maturing peers caught up to and surpassed his athletic accomplishments, the student sought to protect his sense of self-esteem by rationalizing that his lack of success was due to a physical problem. He became obsessed with the thought that he was gradually losing his athletic identity and he lapsed deeper and deeper into a depressed state. His compulsive overtraining and starvation diet failed to produce his image of the "ideal body" that, of course, was unachievable because of his distorted view of reality. Ultimately, this behavior resulted in hospitalization for treatment of an eating disorder and clinical depression. Even a successful senior football season after his psychiatric care could not filter through his distorted perceptions and he could not cope with the thought of participating in another track and field season and having his performance bested by others whom he had once handily beaten. Thus, once again, he engaged in self-protective behavior and sought verification from sportsmedicine professionals. Diagnosis of Tom's condition was possible only through the collaborative efforts of the athletic trainer, physical therapist, sport psychologist, and family physician. Professionals involved in sportsmedicine must be aware of the critical role that highly valued activities like sports play in the psychosocial development of adolescents. To the adult, these activities may seem trivial, frivolous, and removed from the "real world," but to the adolescent, they are an important source of self-esteem during a critical and volatile period of self-concept edification. During a period of awakening sexuality and heightened awareness of their physical being, activities that emphasize the physical aspect of self gain prominence. Those who derive positive experiences benefit from enhanced feelings of physical self-efficacy and self-esteem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Depression and chronic fatigue in the high school student and athlete. 187 14

The effects of carnitine and cobamamide were studied at the unspecific stage of anorexia nervosa treatment. Carnitine and cobamamide accelerated the amelioration of the patients' somatic state (body weight gain, gastrointestinal functions normalization). Experimental psychological technique of involved deciphering discovered that latent fatigue disappeared and mental performance sharply increased under carnitine and cobamamide treatment. Experimental model of anorexia nervosa was used for electron microscopy and morphometry of neocortical tissue structure after starvation period and in feeding rehabilitation with carnitine and cobamamide. These drugs were shown to promote cerebral mass growth, increase in neocortical layers thickness, pyramidal neurons volume, that led to full restoration of normal structure of neocortex. The data provide a basis suitable to recommend carnitineand cobamamide to treat patients with relevant anorexia.
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PMID:[Clinico-experimental substantiation of the use of carnitine and cobalamin in the treatment of anorexia nervosa]. 272 26

1. Exercise results in large alterations in cellular metabolic homeostasis and protein turnovers. Exhaustive exercise (as well as starvation, dystrophy, motor nerve disease) results in myofibrillar degradation and has been associated with the decreased force generating capabilities of muscle at fatigue. 2. Complete protein degradation is accomplished by the combined actions of non-lysosomal and lysosomal proteases and the initial breakdown of myofibrillar protein appears to be non-lysosomal mediated. 3. Current evidence suggests that covalent modification (mixed-function oxidation, formation of mixed disulfides, oxidation of methionine residues and phosphorylation) of proteins may mark them for degradation by rendering them more susceptible to proteolytic attack. 4. The rate of covalent modification can be controlled by the level of stabilizing and destabilizing ligands and by factors affecting the activity of the marking reaction. 5. The activities of individual proteases may be controlled by activators and inhibitors. 6. It is suggested that the large alterations in metabolism (hormonal profiles, energy status, redox status and Ca2+ levels) which accompany exercise serve to activate specific proteases and/or induce covalent modifications which mark specific myofibrillar proteins for subsequent proteolytic attack.
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PMID:Regulation of skeletal muscle myofibrillar protein degradation: relationships to fatigue and exercise. 304 80

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

The effects of oleate starvation on an oleate auxotroph of Escherichia coli K-12 were investigated. Following removal of oleate from the mutant growing in a minimal glycerol-peptone medium, the cells stopped making deoxyribonucleic acid, ribonucleic acid, protein, and phospholipids; they began to die exponentially and finally lysed. During oleate starvation in minimal medium minus peptone, inhibition of macromolecular syntheses and death occurred; however, lysis did not follow. When growth ceased, no further dying was observed. It is shown that none of the early effects (inhibition of macromolecular syntheses and death) can be due to leakiness of the cells, induction of a prophage or a colicin, or lack of energy sources. The cause of inhibition of macromolecular syntheses remained unknown. Since the rate of death was the same as the generation time under different conditions, it appears that death is due to the defective synthesis of some cellular structure (quite possibly, cytoplasmic membrane) during phospholipid deficiency. Lysis was found to require protein synthesis; electron microscopy revealed a peculiar type of "lysis from within"; i.e., the shape of the cells did not change but fragmentation of the inner layer of the cell envelope occurred. The murein was found to be unaltered. Most likely, lysis was a consequence of the cell's attempt to synthesize cytoplasmic membrane with altered phospholipid composition or during phospholipid deficiency. Several membrane functions (respiration, adenosine triphosphate formation, permeability) existing before oleate removal were not lost during starvation. Therefore, general damage to the membrane did not occur, and it could be that most, if not all, described effects were due to defective de novo membrane synthesis.
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PMID:Effects of oleate starvation in a fatty acid auxotroph of Escherichia coli K-12. 489 Dec 68

The effects of 130 h of acute starvation on diaphragm contractility fatigue were studied in isolated rat diaphragm strip preparations with phrenic nerve stimulation. Compared with controls, starvation produced a reduction in body and diaphragm weights. Twitch and tetanic tensions were reduced by starvation; however, when the force was calculated as the strength (normalized for the weight or muscle cross-section area of the diaphragm), no difference was observed between the control and experimental groups. Starvation induced a significant downward shift in the force-frequency relationship, and also increased diaphragm fatigability, but it had no effect on twitch contraction and relaxation time. We conclude that 130 h of acute starvation decreases diaphragmatic force and endurance, but the strength does not change, because of the reducing diaphragmatic mass.
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PMID:Effect of acute starvation on rat diaphragm function. 776 May 28

In most patients with heart failure, an imbalance between energy production and energy utilization leads to a state of chronic energy starvation. This imbalance is due both to increased energy demands caused by overloading of myocardial cells in the failing heart, and to a decreased energy supply caused by reduced perfusion, altered cell architecture, and molecular changes in the hypertrophied heart. Energy starvation has important therapeutic implications in the failing heart. Because the systems that relax the heart are especially sensitive to energetic state, inotropic agents could exacerbate relaxation abnormalities and promote arrhythmias. More important is the likelihood that inotropic agents, which increase cardiac energy expenditure, accelerate cell damage and so worsen prognosis in this condition. Vasodilators and negative inotropic agents, on the other hand, by decreasing energy utilization should improve the balance between energy delivery and energy expenditure in the failing heart.
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PMID:Mechanisms and abnormalities of contractility and relaxation in the failing heart. 802 41

Muscle may suffer from a number of diseases or disorders, some being fatal to humans and animals. Their management or treatment depends on correct diagnosis. Although no single method may be used to identify all diseases, recognition depends on the following diagnostic procedures: (1) history and clinical examination, (2) blood biochemistry, (3) electromyography, (4) muscle biopsy, (5) nuclear magnetic resonance, (6) measurement of muscle cross-sectional area, (7) tests of muscle function, (8) provocation tests, and (9) studies on protein turnover. One or all of these procedures may prove helpful in diagnosis, but even then identification of the disorder may not be possible. Nevertheless, each of these procedures can provide useful information. Among the most common diseases in muscle are the muscular dystrophies, in which the newly identified muscle protein dystrophin is either absent or present at less than normal amounts in both Duchenne and Becker's muscular dystrophy. Although the identification of dystrophin represents a major breakthrough, treatment has not progressed to the experimental stage. Other major diseases of muscle include the inflammatory myopathies and neuropathies. Atrophy and hypertrophy of muscle and the relationship of aging, exercise, and fatigue all add to our understanding of the behavior of normal and abnormal muscle. Some other interesting related diseases and disorders of muscle include myasthenia gravis, muscular dysgenesis, and myclonus. Disorders of energy metabolism include those caused by abnormal glycolysis (Von Gierke's, Pompe's, Cori-Forbes, Andersen's, McArdle's, Hers', and Tauri's diseases) and by the acquired diseases of glycolysis (disorders of mitochondrial oxidation). Still other diseases associated with abnormal energy metabolism include lipid-related disorders (carnitine and carnitine palmitoyl-transferase deficiencies) and myotonic syndromes (myotonia congenita, paramyotonia congenita, hypokalemic and hyperkalemic periodic paralysis, and malignant hyperexia). Diseases of the connective tissues discussed include those of nutritional origin (scurvy, lathyrism, starvation, and protein deficiency), the genetic diseases (dermatosparaxis, Ehlers-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome, homocystinuria, alcaptonuria, epidermolysis bullosa, rheumatoid arthritis in humans, polyarthritis in swine, Aleutian disease of mink, and the several types of systemic lupus erythematosus) and the acquired diseases of connective tissues (abnormal calcification, systemic sclerosis, interstitial lung disease, hepatic fibrosis, and carcinomas of the connective tissues). Several of the diseases of connective tissues may prove to be useful models for determining the relationship of collagen to meat tenderness and its other physical properties. Several other promising models for studying the nutrition-related disorders and the quality-related characteristics of meat are also reviewed.
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PMID:Diseases and disorders of muscle. 839 47

The effects of 4.5 days of acute starvation, either alone or followed by refeeding (ad libitum), on diaphragm contractility, fatigue, and fiber types were studied in male rats. Contractility and fatigue resistance indexes were measured in an in vitro costal diaphragm strip preparation with direct stimulation at 37 degrees C. Compared with controls, starvation produced a 28 +/- 1% (P < 0.001) reduction in body weight and an 18 +/- 4% (P < 0.001) reduction in costal diaphragm weight. Twitch and tetanic tensions (normalized for weight or cross-sectional area) were not reduced by starvation. Starvation produced significant increases in fatigue resistance indexes after a 5-Hz stimulation paradigm but not after a 100-Hz paradigm, supporting the hypothesis that fatigue resistance is dependent on the energy demand of a given paradigm. The proportions of type I and type II fibers were similar between diaphragms of starved and control rats, but the cross-sectional area of type II fibers decreased significantly by 18 +/- 7% (P < 0.01). Thus, despite the significant decrease in diaphragm weight after starvation, contractility was preserved and fatigue resistance was increased (low-output paradigm). This is consistent with the decrease in type II fiber area. Refeeding restored all parameters so that there were no longer significant differences in body or diaphragm weight, contractility, fatigue, or fiber types.
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PMID:Effects of starvation and refeeding on adult male rat diaphragm contractility, fatigue, and fiber types. 845 90


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