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 effect of refeeding on resting energy expenditure (REE) and substrate utilization was studied in 18 hospitalized adolescent girls (aged 12.9-19.1 years) suffering from anorexia nervosa. Changes in body composition were monitored weekly and included weight, fat body mass (FBM), lean body mass (LBM) and total body potassium (TBK). REE was studied weekly by open-circuit calorimetry. Weight gain was noted in all patients (38.2 +/- 5.6 to 44.5 +/- 5.3 kg), involving increased FBM and LBM. REE increased per kg of weight (91.6 +/- 15.1 to 101.7 +/- 18.0 kJ kg-1 d-1) and LBM over the first weeks of refeeding (P less than 0.025) and then stabilized. Substrate utilization showed an increase in carbohydrate and protein utilization (P less than 0.001) during the first few weeks of refeeding. We also studied the thermic effect of food (TEF) in 14 of the 18 subjects. Upon admission the subjects had a reduced TEF (36.4 +/- 24.3 kJ 2 h-1) (P less than 0.001). With refeeding TEF rose to a peak or plateau, then decreased to normal levels (61.9 +/- 36.0 kJ 2 h-1) before discharge from hospital. We conclude that the energy metabolism of adolescent girls adapts to semi-starvation by a reduction in both REE and TEF; with refeeding there is reversal of this adaptive function.
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PMID:Effect of refeeding on the energy metabolism of adolescent girls who have anorexia nervosa. 178 24

Anorexia nervosa (AN) is a syndrome of unknown cause characterized by voluntary starvation. Cholecystokinin has been implicated as a neuroendocrine regulatory factor in control of satiety. Relatively little information is known about gastrointestinal hormone responses to feeding in subjects with anorexia nervosa. In the present studies, we examine fasting and postprandial levels of cholecystokinin (CCK), vasoactive intestinal peptide (VIP) and peptide histidine methionine (PHM) in anorexia nervosa subjects and in control individuals. Results of these studies indicate that plasma CCK response to a liquid meal (Ensure Plus) in untreated AN subjects was distinctly different from that observed in healthy controls, both in terms of temporal pattern of peptide released and the amount of CCK secreted into the circulation. Peak levels of CCK release occurred at 30 min following meal ingestion in AN patients and at 60 min in control subjects. Integrated CCK release in untreated AN patients was approximately twice that measured in control individuals. Renutrition therapy was associated with reversion of the pattern of CCK release to that observed in control subjects. Plasma VIP levels were unchanged following meal ingestion in both control and anorexic subjects. In contrast, PHM levels in AN subjects were significantly greater than that observed in control individuals. The pattern of PHM release following liquid meal ingestion was similar to that observed with plasma CCK; namely, peak release of peptide was observed at 30 min which was significantly greater than corresponding control values (P less than 0.05). In conclusion, these results demonstrate distinctive differences in plasma CCK and PHM levels in response to feeding in AN subjects when compared to control individuals. These findings suggest that the earlier and greater rise in plasma CCK levels in AN subjects following meal ingestion may contribute to the abnormal sensation of satiety in this condition.
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PMID:Cholecystokinin, vasoactive intestinal peptide and peptide histidine methionine responses to feeding in anorexia nervosa. 179 80

Several epidemiological studies as well as clinicians' experience indicate that during the last four decades anorexia nervosa, perfectly described in the 19th century, has become increasingly frequent in industrial societies. In contrast, the disease is said to be extremely rare in traditional societies where it appears only when the life style has been "occidentalized". As a pathology of starvation in a society of abundance, anorexia nervosa lies at the cross-roads of biology and society by referring to two sectors with strong cultural determinations: the ideal body shape and the moral value of food. In a more subtle way, the ever growing incidence of the disease might also coincide with the expansion of such occidental moral values as self-control and individualism and with changes in family structure. Anorexia nervosa may be regarded as a culturally determined illness that "shapes" in a stereotyped mould psychological or even neuroendocrine disorders which vary from one patient to another. This brings it very close to the "culture-bound syndromes" or "ethnic disorders" described by ethnopsychiatrists.
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PMID:[Is anorexia nervosa a cultural disorder?]. 185 92

Patients with anorexia nervosa frequently demonstrate dehydration, electrolyte imbalance and low blood pressure that are secondary to starvation. Hyperactivity of the Renin-Aldosterone system and insensitivity to the pressor effects of exogenous angiotensin II are observed in Pseudo-Bartter syndrome caused by the abuse of diuretics or laxatives and self-induced vomiting, however, little information about the Renin-Aldosterone system has been reported in patients with anorexia nervosa. This study was designed to investigate the secretory function of the Renin-Aldosterone system in anorexia nervosa. The subjects were 13 patients with anorexia nervosa and 6 normal controls. Experiment 1: Angiotensin II infusion test was performed. Blood pressure was measured every 5 minutes, and the samples for plasma renin and serum aldosterone analysis were taken every 15 minutes during infusion test. Experiment 2: Plasma renin activity and serum aldosterone concentration were measured before and after one-hour walking. The results were as follows; (1) Basal plasma renin activity and serum aldosterone concentration in patients were not significantly higher than those in normal subjects. (2) Hypertensive response with elevation of the diastolic pressure during angiotensin II infusion in patients similar to that of normal subjects was observed. (3) Responses of plasma renin activity and serum aldosterone concentration after one-hour walking were significantly greater in patients than in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretory function of the renin-aldosterone system in patients with anorexia nervosa. 201 46

Recent pharmacological studies have more precisely characterised the nature of the inhibitory effect of brain serotonin (5-hydroxytryptamine) on feeding behaviour. Thus, the brain sites and receptors involved have been identified, and a possible physiological role of endogenous serotonin in controlling natural patterns of eating and nutrient selection has been defined. The medial hypothalamus is believed to be a critical location in the mediation of serotonin's action. Specifically, the paraventricular and ventromedial nuclei are known to be involved in controlling energy balance, while the suprachiasmatic nucleus determines circadian patterns of eating. Serotonergic stimulation of these 3 nuclei with exogenous serotonin or drugs that release endogenous serotonin, preferentially reduces carbohydrate intake in naturally feeding animals through satiety mechanisms involved in the termination of feeding. This phenomenon is mediated by serotonin and possibly serotonin receptors, in contrast to serotonin autoreceptors which potentiate feeding possibly by inhibiting serotonin release. The activity of serotonergic function in the medial hypothalamus exhibits a circadian rhythm which is characterised by a peak at the beginning of the active cycle when the motivation to eat is strongest and is triggered by deficits in energy stores. At this time, carbohydrate is found to be the naturally preferred macronutrient, and it appears that serotonin becomes most activated under these conditions to terminate the carbohydrate-rich meal, possibly by activating satiety neurons localised in the medial hypothalamus. In this process, serotonin may interact antagonistically with noradrenaline (norepinephrine) and its alpha 2-noradrenergic receptors that normally function to enhance carbohydrate intake at the onset of the natural feeding cycle. Moreover, while inducing satiety for carbohydrate, serotonin may also play a role in switching the animal's preference towards protein. The regulation of this macronutrient is closely linked to that of carbohydrate, and it is normally preferred in the second meal of the natural feeding cycle. Most of the pharmacological evidence to date generally supports the hypothesis that disturbances in serotonin function occur in eating disorders. Decreases in plasma tryptophan, urinary 5-hydroxyindoleacetic acid (5-HIAA), platelet serotonin binding and basal cerebrospinal fluid 5-HIAA in anorexia nervosa normalise upon weight restoration and appear to be starvation effects. These alterations in serotonergic function may however perpetuate the symptomatology of anorexia nervosa once the illness is set in motion. Some drugs which in part affect serotonergic function facilitate weight gain in conjunction with an integrated psychotherapeutic and behavioural programme. Patients with bulimia nervosa, regardless of the presence of anorexia nervosa or major depression, who have been relatively weight stable and free of binge/vomit episodes for at least 3 weeks, have significantly blunted prolactin responses to the serotonin agonists. These findings indicate that post-synaptic responsiveness in hypothalamic-pituitary serotonergic pathways is reduced in bulimia. Similar alterations in other serotonin pathways at or above the level of the hypothalamus may contribute to binge eating and other behavioural symptoms in bulimic patients. The clinical response to several psychotropic agents known to potentiate serotonergic transmission further substantiates a serotonin dysregulation hypothesis of bulimia nervosa.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of serotonin in eating disorders. 219 74

The internist plays a critical role in the care of eating disorder patients, especially in the management of the life-threatening medical complications of these conditions. In anorexia nervosa, the immediate danger is related to the effects of voluntary starvation, including hypophosphatemia, bone marrow failure, cardiac decompensation, and shock. Patients with bulimia nervosa more often experience severe fluid and electrolyte abnormalities resulting in hypovolemia, secondary hyperaldosteronism, depletion of total body potassium, and cardiac arrhythmias. Immediate management of medical complication and correction of nutritional deficits are necessary before patients can benefit from psychotherapy. The need for continued involvement of the internist in the ongoing care of the eating disorder patient is stressed. The high mortality and the likelihood of chronicity without early intervention underscore the need for early recognition and skilled management of eating disorders.
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PMID:Medical complications of anorexia nervosa and bulimia nervosa. 220 58

We have studied the effect of acute short-term starvation (in 9 patients) and of prolonged caloric deprivation (in 10 patients with anorexia nervosa), on cell-mediated cytotoxicity (CMC). CMC became severely depressed after six days on a very low caloric diet (1.2 +/- 1.4 vs. 7.0 +/- 2.9 lytic units/10(6) cells; P less than 0.01). CMC was also low in our patients with anorexia nervosa compared to a matched control group (3.3 +/- 1.7 vs. 10.0 +/- 3.0 lytic units/10(6) cells; P less than 0.01) and increased in most of the patients studied (five cases) after the first 3-4 weeks of refeeding in correlation with weight gain. Dietary deprivation may lead to a significant impairment in cell-mediated cytotoxicity, which appears to be reversible after refeeding.
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PMID:The effect of different nutritional states on cell-mediated cytotoxicity. 237 24

The suppressive effect of dexamethasone (Dex) on plasma cortisol and beta-lipotrophin (beta LPH) was investigated in patients with anorexia nervosa. Dex was given either orally, 1 mg at 2400 h, with blood sampling at 0800 h on the days before and after Dex, or by i.v. infusion starting at 1100 h (1 mg/h) for 4 h with sampling at 0800, 1100, 1500, 2000 and 2400 h and at 0800 h the following day. The plasma cortisol and beta LPH levels during oral or i.v. Dex administration were compared between patients and normally menstruating women of normal weight. The results showed that Dex administration depressed cortisol significantly (P less than 0.0001) during oral or i.v. infusion in most patients, without, however, suppressing it entirely as is the case in normal women. Moreover, during i.v. Dex infusion, the concentrations of cortisol escaped suppression and were higher than in normal women (less than 50 nmol/l) by 0800 h on the day following infusion. In the patients who were reinvestigated after re-feeding and weight gain (n = 9), a normal suppression of cortisol in response to i.v. Dex infusion was observed in only five cases and a slight failure to suppress, although concentrations were lower than before refeeding, was still evident in four. We concluded that, in anorexia nervosa, cortisol concentration rapidly escapes suppression by Dex administration, and that this escape is not related to the degree of starvation.
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PMID:Rapid escape of cortisol from suppression in response to i.v. dexamethasone in anorexia nervosa. 240 Oct 98

Patients with anorexia nervosa (AN) exhibit neuroendocrine abnormalities that may result solely from emaciation or may reflect defective endocrine mechanisms which are intrinsic to disordered eating even in the absence of starvation. To distinguish these possibilities, we have studied indices of hypothalamic-pituitary-gonadal (HPG) function in 9 patients with AN, 12 normal weight patients with bulimia and recent or current oligomenorrhea, and 8 normal weight controls. Measurement of 24-hour luteinizing hormone (LH) secretion with 30-min sampling revealed significantly fewer LH secretory spikes and a trend toward lower mean 24-hour LH levels in both bulimic and anorectic patients than in controls. Stimulation with gonadotropin releasing hormone produced elevated LH responses in the bulimic group and blunted LH responses in the anorectic group. Stimulation with estradiol revealed diminished LH augmentative responses and a trend toward diminished follicle stimulating hormone augmentative responses among bulimic as well as AN patients compared to controls. In each instance, the bulimic group tended to show within-group heterogeneity, with some individuals falling within the AN range. These findings suggest that HPG axis abnormalities in eating disordered patients cannot entirely be attributed to emaciation and that factors other than subnormal weight contribute to disturbed hypothalamic-pituitary functioning in these patients.
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PMID:Hypothalamic-pituitary-gonadal function in anorexia nervosa and bulimia. 250 Jun 76


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