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)

The present study investigated the application of female rats with activity stress as an animal model for anorexia nervosa. Young female rats were singly housed in activity-wheel cages with food-restricted schedule (2, 3, or 4 h of food availability per day) for 3 weeks. Estrous cycle, body weight, food intake, and wheel revolution were recorded daily. Gastric pathology was also observed using the endoscopic technique. Rats that were subjected to either a 3- or 4-h feeding schedule exhibited the cessation of estrous cycle, loss of body weight, and suppression of food intake. These animals also showed a remarkable increase in running activity. However, they had no gastric lesions throughout the experimental period. On the contrary, the 2-h feeding schedule elicited severe gastric lesions and high mortality. The results suggest that behavioral and physiological changes of the young female rats with 3 or 4 h feeding share some symptoms of anorexia nervosa, although their anorexia is not self starvation.
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PMID:Feeding conditions and estrous cycle of female rats under the activity-stress procedure from aspects of anorexia nervosa. 159 81

The appropriate choice of treatment for infants with diarrhea has long provoked debate. Growth of infants with diarrhea is adversely affected by associated diseases including anorexia, malabsorption, catabolic response to infection, and iatrogenic starvation. To prevent the negative effects of diarrhea on the nutrition of infants, continued feeding during the active and early convalescent phases has been recommended. Although this concept is not new, until recently it has been little used in the treatment of diarrhea. In this article we examine the current knowledge about, and trends in, feeding infants with diarrhea. We will discuss treatments for the well-nourished infant with acute diarrhea, the infant with prolonged diarrhea, and the malnourished infant. Information regarding the use of local staples will also be provided.
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PMID:Nutritional therapy for infants with diarrhea. 209 32

Anorexia nervosa and bulimia nervosa are eating disorders with distinct clinical presentations. Reduced caloric intake, a hallmark of both disorders, is manifested by self-induced starvation in anorexia and by binge eating and gastrointestinal purging in bulimia. Treatment includes nutritional intervention, psychotherapy and pharmacotherapy in either the ambulatory or the hospital setting.
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PMID:Anorexia and bulimia. 218 33

The time course of the behavior of rats fasted for 24 h was analyzed with observation starting either 10 or 60 min after the i.c.v. administration of ACTH-(1-24) (4 micrograms/animal). The anorectic effect of this peptide was direct and specific because it could be dissociated in time from the grooming-inducing effect. The effect is a central one, not linked either to an interaction with the peripheral feeding-regulatory system, or to the release of adrenal steroids. ACTH-(1-24), like corticotropin-releasing factor (CRF), is capable of antagonizing the stimulation of feeding seen during starvation, insulin (10 IU/kg s.c.)-induced hypoglycemia, stimulation of GABAergic (muscimol, 250 ng/rat i.c.v.), noradrenergic (norepinephrine, 20 micrograms/rat i.c.v.) or opioidergic systems. The data suggest that both CRF and ACTH may be considered as putative mediators in the production of stress-induced anorexia.
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PMID:Inhibition of feeding by ACTH-(1-24): behavioral and pharmacological aspects. 219 23

We have developed a murine model of wasting by injecting intracerebrally cells which continuously secrete h-cachectin/TNF (CHO-TNF) to: (a) determine the effects of cachectin/TNF produced continuously in the central nervous system (CNS), and (b) compare the metabolic effects of cachectin/TNF-secreting tumor in the brain to the cachexia caused by CHO-TNF tumor in peripheral tissue (IM). Intracerebral CHO-TNF tumors produced increased serum h-cachectin/TNF levels with lethal hypophagia and weight loss (mean survival time of 11 d); these changes were not observed in association with nonsecretory control brain tumors. The metabolic consequences of intracerebral cachectin/TNF production were indistinguishable from acute, lethal starvation: whole-body lipid content was decreased significantly but protein was conserved. Although intramuscular cachectin/TNF-secreting tumors caused similar increases of serum h-cachectin/TNF levels, profound anorexia did not develop; wasting developed after a longer period of tumor burden (50 d) with classical signs of cachexia (i.e., anemia and depletion of both protein and lipid). These studies provide a reproducible animal model of site-specific cytokine production and suggest that, regardless of serum levels, cachectin/TNF produced locally in brain influences both the rate of development of wasting and its net metabolic effects.
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PMID:Metabolic effects of cachectin/tumor necrosis factor are modified by site of production. Cachectin/tumor necrosis factor-secreting tumor in skeletal muscle induces chronic cachexia, while implantation in brain induces predominantly acute anorexia. 225 57

Patients with anorexia nervosa have neuroendocrine and behavioral alterations that starvation and weight loss are thought to cause, or contribute to, since they are reversed by weight restoration. We have found that anorexics have starvation-related disturbances of neuropeptide Y (NPY), corticotropin-releasing hormone (CRH), and beta-endorphin, as determined by their measurements in cerebrospinal fluid. The relationship between these neuropeptides and several symptoms in anorexia, together with findings in experimental animals, raise a possibility that changes in the activity of these neuropeptides contribute to neuroendocrine and behavioral alterations in anorexia. Specifically, a disturbance of central nervous system CRH activity is likely to be responsible for hypercortisolemia, while a disturbance of central nervous system NPY may contribute to amenorrhea. In addition, disturbances of these neuropeptides could contribute to other symptoms such as increased physical activity, hypotension, reduced sexual interest, depression, and pathological feeding behavior.
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PMID:Contribution of CNS neuropeptide (NPY, CRH, and beta-endorphin) alterations to psychophysiological abnormalities in anorexia nervosa. 253 90

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

The role of T-2 toxin-induced gastrointestinal lesions in T-2 toxin-enhanced resistance to listeriosis in mice was evaluated. The T-2 toxin-induced lesions did not cause a starvation effect sufficient to enhance resistance to listeriosis. Administration of polymyxin E markedly reduced the gram-negative intestinal microflora and did not eliminate the toxin-induced resistance to listeriosis. The T-2 toxin did not cause an increased expression of Ia surface antigens on peritoneal macrophages. Thus, toxin-induced anorexia and starvation or absorption of gram-negative intestinal bacteria and endotoxins through toxin-induced gastrointestinal lesions did not account for the enhancing effect of T-2 toxin on resistance to Listeria monocytogenes infection in mice.
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PMID:T-2 toxin-enhanced resistance against listeriosis in mice: importance of gastrointestinal lesions. 311 16

The morphologic features of the anterior pituitary gland were studied by immunohistologic methods in 12 patients who had died of complications of anorexia nervosa, 4 patients who had died while on a "crash diet", 13 patients who had died of organic disease associated with inanition, and 5 age- and sex-matched control subjects who had been involved in sudden fatal accidents. All known pituitary hormones were found to be present. Abnormalities noted in both the patients with anorexia and those with organic inanition included relative hypogranulation of adrenocorticotropic and, to a lesser extent, growth hormone cells. These changes are of unknown importance but are likely the result of starvation in that they were not observed in patients on a "crash diet" or in control patients. We conclude that no specific or etiologic abnormalities are present in the pituitary glands of subjects with anorexia nervosa and that the altered secretion of adenohypophyseal hormones often noted in patients with this disorder cannot be attributed to a primary pituitary disorder.
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PMID:Anorexia nervosa: an immunohistochemical study of the pituitary gland. 333 38

A novel model of nutritionally induced hypertension in the rat is described. Dietary obesity was produced by providing sweet milk in addition to regular chow, which elicited a 52% increase in caloric intake. Despite 54% greater body weight gain and 139% heavier retroperitoneal fat pads, 120 days of overfeeding failed to increase systolic pressure in the conscious state (125 +/- 8 vs. 121 +/- 4 mmHg in chow-fed controls) or mean arterial pressure under urethan anesthesia (71 +/- 4 vs. 63 +/- 3 mmHg). In contrast, mild hypertension developed in intermittantly fasted obese animals (a 21-mmHg increase in systolic blood pressure measured in the conscious state and a 16-mmHg increase in mean arterial pressure under anesthesia relative to chow-fed controls). The first 4-day supplemented fast was initiated 4 wk after the introduction of sweet milk, when the animals were 47 g overweight relative to chow-fed controls. Thereafter, 4 days of starvation were alternated with 2 wk of refeeding for a total of 4 cycles. A rapid fall in systolic blood pressure (12 +/- 2 mmHg at 2 days) accompanied the onset of supplemented fasting and was maintained thereafter (2.7 +/- 2.6 mmHg further decrease during the latter half of the fast). With refeeding, blood pressure rose precipitously (13 +/- 3 mmHg in the 1st 2 days), despite poststarvation anorexia. Blood pressure tended to rise slightly over the remainder of the realimentation period (5.2 +/- 2.8 mmHg). After the 4th supplemented fast, hypertension was sustained during 30 days of refeeding. Cumulative caloric intake in starved-refed rats fell within 2% of that in chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Refeeding hypertension in dietary obesity. 333 69


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