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)

1. Clinical and necropsy observations in lepromatous leprosy associated with severe emaciation and accompanying hypoproteinemia suggest that protein deprivation may be of pathogenic significance in the ulcerative phenomenon that is designated "Lazarine leprosy". 2. An experimental utilizing Wiersung rats infected with Mycobacterium lepraemurium and maintained on a protein-free diet was developed for the purpose of studying the effect of protein starvation on the course of chronic mycobacterial disease similar to lepromatous leprosy with respect to pathogen and host inflammatory response. 3. It was possible to maintain the experimental animals on a protein-free diet for up to 18 weeks of concomitant M. lepraemurium infection. This was long enough for the infection to disseminate to a degree that was evident in control animals only several weeks later. 4. The protein-deprived animals showed decreased inflammatory response to the pathogen, presented more rapid dissemination of the infection and harbored more bacilli per macrophage than did animals similarly infected but maintained on a protein adequate diet. This indicates impairment of native cellular immunity by protein deprivation through decrease in ability of macrophages to inhibit bacillary multiplication. 5. There was no evidence of impairment of macrophage ability to phagocytose the pathogens. 6. Morphologically the increased dissemination of pathogens and decrease in inflammatory response was similar to the increase in number and extent of visceral lesions seen in Lazarine leprosy. Decreased ability to dispose of the infecting bacilli was similar in the two models, human and animal. The animal model does not, as does lepromatous leprosy, involve the skin in the infection. Hence comparable ulcerative phenomena were not replicated in the animals. 7. It is suggested that Lazarine leprosy may result from enhanced lepromatous leprous infection occurring as a result of protein malnutrition. The pathogenic mechanism appears to be impairment of cellular immunity probably enhanced by concomitant impairment of humoral antibody immunity resulting also in decreased resistance to pyogenic and other secondary pathogens. The tissue edema attendant on decreased serum osmotic pressure due to lowering of the serum protein fractions enhances the probability of ulceration.
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PMID:The role of protein malnutrition in the pathogenesis of ulcerative "Lazarine" leprosy. 82 11

Muscle protein catabolism has been evaluated using the excretion of urinary 3-methylhistidine (3-MEH) is six normal male and six normal female subjects and in four surgical patients, two of whom developed febrile episodes during the course of their study. In addition, their nutritional status was also evaluated using percentage body weight losses before hospital admittance, creatinine-height ratios, and, in two patients, serum alkaline ribonuclease levels. The results indicate that: 1) prolonged starvation may produced decreased 3-MEH excretion because of an adaptive diminution of muscle breakdown in sustained starvation, decreased 3-MEH excretion also may simply reflect diminished lean body mass, 3-MEH excretion may be increased above basal levels because of superimposed stresses such as fever, and the acute phases of starvation produce increased levels of 3-MEH excretion until adaptive mechanisms occur; 2) creatinine-height ratios are low in starvation, and increase not only with improved nutrition but in response to fever and stress of operation, even when these are superimposed on malnutrition; and 3) alkaline RNAase levels are elevated in malnutrition and decrease with improved nutrition but in response to fever and stress of operation, even when these are superimposed on malnutrition; and 3) alkaline RNAase levels are elevated in malnutrition and decrease with improved nutrition. The enzyme may also be elevated by the stress of operations.
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PMID:Muscle protein catabolism in the septic patient as measured by 3-methylhistidine excretion. 88 85

The effects of folate deficiency, generalized malnutrition, and alcohol ingestion on jejunal transport, mucosal uptake, and reduction of folic acid were evaluated in rats. As measured by an everted gut sac technique, a folate-deficient diet fed ad libitum did not alter transport or mucosal uptake of folate. Partial starvation, which was produced in rats pair-fed with animals ingesting ethanol, increased jejunal folate transport and mucosal uptake in animals ingesting either a folate-deficient or control diet. A 20% ethanol ingestion by rats consuming folate-deficient or control diets resulted in transport and mucosal uptake rates intermediate in value compared to those from ad libitum fed and pair-fed groups. No differences in reduction of folic acid were found. These results suggest that folate depletion and ethanol ingestion, alone or in combination, do not affect the ability of the rat jejunal to transport folate but that partial starvation results in an increase in folate transport activity.
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PMID:Effect of folate deficiency and ethanol ingestion on intestinal folate absorption. 92 Jun 93

Cardiac: Cardiac protein synthesis is influenced by the state of nutrition with reduction of cardiac size in starvation. Ethanol per se may not affect this synthesis directly, but the metabolite of ethanol, acetaldehyde, profoundly decreases normal protein synthesis in the heart in vitro. The interference with the synthetic process may play a role in the ultimate cardiomyopathies of malnutrition and alcoholism. Hepatic: In vivo albumin synthesis is sensitive to environment, oncotic pressure, normal balance, nutrition, as well as toxins and state of health. Thus, to study the acute effects of alcohol alone, it was necessary to employ the isolated perfused liver. Fasting reduced albumin synthesis 50%, with loss of RNA and a disaggregation of the endoplasmic membrane bound polysome. Tryptophan, arginine and ornithine added to the perfusate at a final concentration of 10 mM reversed these findings. Alcohol likewise reduced albumin synthesis; disaggregates the bound polysome without a marked loss of RNA. Ornithine, arginine and tryptophan are able to reverse this loss in albumin synthesizing capacity. The combination of fasting and alcohol, while not lowering albumin synthesis below that seen with either stress alone, prevents the recovery from either stress.
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PMID:Effects of ethanol on protein synthesis. 109 51

The high prevalence of low-birthweight (less than or equal to 2,500 gm) babies in many poor communities is a major public health problem. Studies in humans in situations of acute starvation suggest an effect of maternal nutrition on birthweight, but less clear results appear under situations of moderate maternal malnutrition. We studied the effects of food supplementation during pregnancy on birthweight in four rural villages of Guatemala, in which two types of supplements were distributed: protein-caloric and caloric. The caloric supplementation increased the total caloric intake during pregnancy. In both supplements, the amount of calories supplemented during pregnancy showed a consistent association with birthweight. In the combined sample the proportion of low-birthweight babies in the high-supplement group (G greater than or equal to 20,000 supplemented calories during pregnancy) was 9% compared with 19% in the low-supplement group (less than 20,000 supplemented calories during pregnancy). The relationship between caloric supplementation and birthweight (29 gm of birthweight per 10,000 supplemented calories) was basically unchanged after controlling for the maternal home diet, height, head circumference, parity, gestational age, duration of disease during pregnancy, socioeconomic status, and different rates of missing data. Moreover, a similar association was found in consecutive pregnancies of the same mother. We concluded that caloric supplementation during pregnancy produced the observed increase in birthweight.
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PMID:Effect of food supplementation during pregnancy on birthweight. 116 55

Unless the nutrition community intervenes in national and international policymaking, the world could well be headed for serious trouble with deaths from starvation on a consequential scale. There has been near-total dissociation between agricultural planning policies and food distribution and nutritional needs of populations. Unfortunately, the nutrition community is out of the mainstream of forces which affect nutritional status and which produce the macro-decisions. Why? Perhaps the professionals have too narrow a view of their role; although malnutrition is a health problem, the solution is not necessarily one of health delivery. Perhaps they don't seriously wish to be involved with policy change and the work it entails. Perhaps, by being unable to achieve consensus within their own ranks, they have generated a lack of credibility. The nutrition community needs to recognize a broader scope for nutrition and to take new approaches in advocacy directed to education policy-makers. No one else can play this role with authority.
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PMID:Fear of trying. 125 73

The effects of ageing and starvation on the rat myocardium were studied by morphometric methods. Since cardiac muscle is a tissue with a high level of anisotropy, methods based on the concept of vertical planes were used to describe quantitative alterations in the rat myocyte both at the cellular and ultrastructural level. During starvation rapid and important changes were noted, particularly in the transverse dimension of cells and organelles. The most striking change, however, was the immediate dilatation of the myocyte T-system, reflecting an adaptive interaction between the intra- and extracellular environment. At the same time exocytosis of intracellular components into the extracellular space of the T-system was observed. The ratio of mitochondria to myofibrils decreased progressively during starvation. Such a decrease, in general, may reach a point when cellular energy supply becomes compromised. A comparison between different regions of the heart showed no differences and it can be concluded that the morphological changes during starvation are the same, and equally distributed, in both ventricles. The changes described in the aged rat heart point in the direction of a hypertrophy of the aged myocyte. This leads to a lower ratio between surface and volume which finds its representation at the subcellular level in a more spherical shape of nuclei and mitochondria. Unlike what is seen in malnutrition, the mitochondrial/myofibril ratio is higher in the older rat. From the morphological point of view, the atrophy of malnutrition and the hypertrophy of ageing are opposed, but in both there is a change in the relationship of the myocyte to its environment which directly influences the substrate exchange capacity. This tends to protect the myocyte in starvation but jeopardizes the older cell.
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PMID:Effect of ageing and malnutrition on rat myocardium. I. The myocyte. 141 85

The modulating effects of ageing and malnutrition on rat myocardium were studied morphometrically with respect to the microvasculature. An increase in capillary density together with a decrease in capillary lumen cross-sectional area was noted during starvation. The important changes seen in the myocyte T-system were paralleled by a decreased diffusion distance for oxygen from the capillary lumen to the mitochondrion. The changes described in the aged rat heart point to an altered inter-relationship between parenchyma and vascularization with a lower capillary volume fraction and a greater diffusion distance from the capillary lumen to the mitochondrion; this is caused by hypertrophy of the aged myocyte. This reduction in capacity to exchange substrates is further reduced by the less developed T-system in the older myocyte.
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PMID:Effect of ageing and malnutrition on rat myocardium. II. The microvasculature. 141 86

Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses.
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PMID:Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig. 141 61

Data from a case-control study of Alzheimer's disease (AD) were analysed in relation to age of onset and familial/sporadic status. The analyses were restricted to environmental exposures which might injure the brain. Later-onset AD was found to be positively associated with starvation/malnutrition and with nose-picking and negatively with analgesics, while earlier-onset was associated with physical underactivity and nervous breakdown more than 10 years before. Sporadic AD was associated with starvation/malnutrition and with head injury. These analyses merit replication in other large case-control studies of AD.
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PMID:Environmental risk factors for Alzheimer's disease: their relationship to age of onset and to familial or sporadic types. 161 10


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