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

Morphological changes in rat sciatic nerve (SN) and plantar nerve (PN) induced by a thiamine deficient diet (TDD) and administration of oxythiamine (OT: 4 mg/100 g X 6 days) were observed, and thiamine (T) levels in rat nerve were simultaneously determined. Body weight gain ratio in rats which received OT fed a TDD (OTD group) was much reduced, and anorexia and ataxia were recognized in this group. Rats fed a regular diet, whose weights were restricted to be the same as those in the OTD group (EWC group), showed the symptoms of starvation. T levels of the SN and PN in the OT group, OTD group, and rats fed a TDD (TDD group) were reduced, but in the EWC group, T levels were the same as those in the control group (C group). There were myelin folds and myelin oboids in the EWC group, and these were recognized before axonal degeneration. In the TDD group, an increase in the number of mitochondria (Mit) was seen in the myelinated axon (MAx). In the TDD group, an increase in the number of mitochondria (Mit) was seen in the myelinated axon (MAx). In the OT and OTD groups, axonal degeneration (increase in the number of Mit, appearance of degenerated Mit, axonal shrinkage, and disappearance of neurofilament and neurotubule) was observed in the MAx. Degeneration of the MAx caused by TDD and OT was more severe in the PN than in the SN. Since these changes progressed from the peripheral nerve to the centripetal one, these changes in OTD group might be dying-back polyneuropathy.
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PMID:[Effect of oxythiamine on rat peripheral nerve. --Morphological changes in sciatic nerve and plantar nerve of thiamine deficiency-- (author's transl)]. 709 52

Rabbits parasitized by Obeliscoides cuniculi were used as models for stomach worm parasitism in ruminants. A 3 X 4 randomized complete block design containing three levels of of infection (NI, no infection; LI and HI, infections produced by 1,800 and 30,000 larvae, respectively) and four levels of diet (PC, high protein and carbohydrate; pc, low protein and carbohydrate; Pc, high protein, and low carbohydrate; pC, low protein and high carbohydrate) was replicated four times. Mean weight gains for rabbits on diets pc or PC were not influenced by infection level, whereas LI rabbits on diets Pc and pC gained as well as the NI animals and more than the HI ones. Only HI rabbits exhibited anorexia. NI and LI rabbits has positive feed conversion efficiencies, whereas those of HI rabbits were negative. The apparent digestibilities of organic matter, protein, and ash in rabbits with different infection levels varied with diet. Daily nitrogen balances were positive. The changes in concentrations of amino acids in the plasma typically associated with systemic, fever-producing infections or with starvation or protein-calorie malnutrition did not occur in infected rabbits. Only the high level infections produced adverse effects on productivity. These effects occurred on diets pc, Pc and pC and were mediated by anorexia.
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PMID:Metabolic effects of infection by the stomach worm Obeliscoides cuniculi in rabbits fed diets varying in nutritive quality. 713 Oct 89

A discussion of "Anorexia Nervosa and the Psychotherapeutic Hospital," by Ian Story Ph.D. "Anorexia Nervosa" is a misnomer. "Anorexic" patients do not suffer from loss of appetite but actively pursue self-starvation and are frantically preoccupied with food, and even more with their size and shape. It is not an illness of weight and nutrition but a desperate effort to establish a sense of control to counteract deficits in the sense of effectiveness and the self-concept. After a childhood of overconformity, these patients are ill prepared to meet the demands for independence and self-assertion that growing up implies. Traditional treatment has emphasized the restitution of weight, which, however, is insufficient for cure. For effective treatment, reparation of the underlying personality deficits is essential. Story's paper on the therapeutic hospital describes the desperate plight of chronic anorexic patients in whose early treatment this important factor had been neglected.
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PMID:Treatment in anorexia nervosa. 715 18

Weight loss is a potent stimulus to food intake in normal individuals. The persistence of anorexia in wasting disorders, therefore, implies a failure of this adaptive feeding response. We describe a model for the normal hypothalamic response to starvation composed of the stimulation of neuronal pathways that promote energy intake and storage coupled with the inhibition of pathways that exert opposing effects. This model provides a framework for investigating disturbances of the normal hypothalamic response to weight loss and suggests a specific mechanism by which cytokines contribute to wasting in acquired immune deficiency syndrome and other cachexic disorders.
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PMID:Hypothalamic response to starvation: implications for the study of wasting disorders. 750 22

Rabbits are not usually susceptible to intestinal Shigella infection without extensive pretreatment, including starvation and administration of antimicrobial, antimotility, and toxic agents (carbon tetrachloride). Most animals infected this way die rapidly and do not always develop colonic lesions and signs of dysentery. We describe here a successful experimental infection in the adult rabbit which does not require preparatory treatment and which reproduced characteristic features of human shigellosis. Unstarved, untreated adult rabbits were infected by direct inoculation of virulent Shigella flexneri 2a (10 ml of 10(7) bacteria per ml) into the proximal colon after ligation of the distal cecum (cecal bypass). Within 24 h of infection, most inoculated animals consistently developed clinical dysentery, characterized by liquid stool mixed with mucus and blood, leukocytosis, anorexia, and weight loss. Histologically, there were edema, exudation, superficial ulceration, and polymorphonuclear infiltrations in the lamina propria; crypt abscess formation; focal hemorrhages; and the presence of immunohistochemically stained S. flexneri in the colonic mucosa. Successful bacterial colonization was indicated by the isolation of the challenge strain of S. flexneri 2a from the colonic contents. None of the control rabbits challenged with nonvirulent S. flexneri or without cecal bypass developed dysentery or colitis. We conclude that successful Shigella infection can be induced by direct colonic inoculation with virulent S. flexneri 2a in adult rabbits without starvation and pretreatment. The colitis is dependent on the virulence of the bacteria and on the cecal bypass. This model should be useful in studies of the immunopathogenesis of Shigella infection.
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PMID:Development of an improved animal model of shigellosis in the adult rabbit by colonic infection with Shigella flexneri 2a. 759 Oct 70

Fifty-five eating-disordered women and 16 normal controls participated in this study to determine whether olfactory function is altered in patients with food-restricting anorexia, anorexia with bulimic features, and bulimia nervosa. Olfactory function was assessed using the University of Pennsylvania Smell Identification Test and by determining phenyl ethyl alcohol odor detection thresholds. Only the very low-weight anorexics showed impairments in their identification and detection of odors. This group's olfactory function did not improve from admission to discharge despite significant weight gain. Although, overall, smoking had only a minor influence on olfactory function, the very low-weight anorexic smokers had the lowest scores of all subjects. Since higher-weight anorexics did not show such impairments, the results suggest that the severe and prolonged starvation experienced by the very low-weight anorexics caused or contributed to intractable deficits in the olfactory system and that these deficits are compounded by smoking.
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PMID:Olfactory dysfunction in anorexia and bulimia nervosa. 767 Apr 45

Anorexia, net proteolysis of skeletal muscle and consumption of body fat are hallmarks of the cachexia syndrome associated with chronic disease states. While inanition contributes to cachexia, this wasting diathesis has little in common with simple starvation. The cachexia syndrome is characterized by progressive weight loss and depletion of lean body mass in excess to that resulting from comparable caloric restriction. Accelerated mobilization and consumption of host protein stores from peripheral tissues occurs to support gluconeogenesis and acute phase protein synthesis [1, 2]. In contrast, simple starvation is associated with a relative sparing of lean tissue with the preferential consumption of fat. While the clinical manifestations of cachexia are readily apparent, identification of the specific mechanisms responsible for the development of cachexia remains an enigma. In recent years, interest has focused on the role that the immune system plays in the development of cachexia. Investigators initially hypothesized that the chronic production of two inflammatory cytokines, tumour necrosis factor alpha (TNF alpha) and/or interleukin-1 (IL-1), could explain the host non-specific responses resulting in cachexia [3-5]. Other pro-inflammatory cytokines, including interleukin-6 (IL-6) [6, 7] and interferon-gamma [8, 9], have been more recently proposed to be involved in this complex process. Although no consensus exists for the exclusive role of any one cytokine in the pathogenesis of cachexia, there is growing acceptance that the progression of cachexia results in part from the inappropriate release of one or more pro-inflammatory cytokines [10, 11]. In the present review, the current role of TNF alpha as a mediator of cachexia is examined.
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PMID:Tumor necrosis factor and cachexia: a current perspective. 788 18

The autosomal recessive lethal anorexia mutation in mice (anx/anx) causes starvation in preweanlings. In addition, this murine neurodevelopmental mutant shows other distinct phenotypic characteristics and dysfunctional behaviors. Previous studies strongly suggested that the mutation results in elevated serotonergic stimulation, because these traits are characteristic of such overstimulation and because brain serotonin is believed to have an inhibitory effect on feeding behavior. In this report, we show extensive serotonergic hyperinnervation in normal target fields (hippocampus, cortex, olfactory bulb and cerebellum) of mutant mice. Despite the extensive hyperinnervation, the normal laminar organization of the brain was retained. The specificity of the mutation to the serotonergic system was confirmed by demonstration of normal catecholaminergic innervation in the central nervous system (CNS), and this specificity was especially striking in a common target field, the cerebellum. Serotonergic hyperinnervation in these mutant preweanling mice may represent the underlying etiology of increased serotonergic stimulation which leads to anorexic starvation, abnormal behavior, and premature death.
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PMID:Drastic and selective hyperinnervation of central serotonergic neurons in a lethal neurodevelopmental mouse mutant, Anorexia (anx). 798 37

Twenty patients with anorexia nervosa and a body weight below 60% of the standard weight were studied. One died of starvation; the others survived. Four patients, including the deceased, had such severe weakness that they could not sit up without support, and another five could sit up only from a lateral position. Serum albumin or hemoglobin levels at the beginning of therapy could not be used for nutritional assessment because of dehydration, while increased blood urea nitrogen was associated with acute illness. The present results together with data from previous studies of fatal anorexia indicate that the risk of mortality may be quite low when body weight is above 60% of the standard. We suggest that gross muscle weakness in addition to body weight for height can be a valuable indicator to assess the criticalness in anorexia nervosa.
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PMID:Assessment of emaciation in relation to threat to life in anorexia nervosa. 801 84

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.
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PMID:Nutrition support and the human immunodeficiency virus (HIV). 811 86


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