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

Rats fed on a restricted feeding (RF) schedule of 4 h day-1 to produce a 15-20% reduction in body weight were killed before (starved) and after (fed) the presentation of food on the sixth day to compare 5-hydroxytryptamine (5-HT; serotonin) metabolism and synthesis rate in the hypothalamus with freely feeding (FF) controls. The RF rats showed lower 5-HT concentration and synthesis rate than FF controls. Restricted feeding did not decrease tryptophan concentration in the hypothalamus. However, RF-fed rats had lower tryptophan concentration than RF starved rats. 5-HIAA concentration was comparable in RF fed rats and FF controls but higher in RF starved rats. Possible implications of the findings in the pathogenesis of the food deprivation/starvation-related disease anorexia nervosa are discussed.
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PMID:Food restriction decreases serotonin and its synthesis rate in the hypothalamus. 881 22

Eating disorders are associated with numerous biological perturbations; however, sorting out cause from effect is difficult. Neuroendocrine and metabolic abnormalities are seen in both anorexia nervosa and bulimia nervosa, but they have not been described in binge eating disorder, in which neither starvation nor compensatory behaviors are present. Although these findings may reflect biologic differences among subgroups of binge eaters, an alternative explanation is that many of the biological correlates of binge eating are the result of metabolic derangement secondary to starvation and/or purging. The identification of binge eating disorder provides an opportunity to study the causes and concomitants of binge eating in the absence of compensatory behaviors.
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PMID:Biological correlates of binge eating. 882 May 23

Using positron emission tomography and (18-F)-fluorodeoxyglucose, we studied cerebral glucose metabolism in 10 anorectic girls within their underweight state and after weight gain. Ten age- and sex-matched healthy volunteers were used as controls. Both groups were scanned during rest, eyes closed and with low ambient noise. In absolute values, the underweight anorectic patients, when compared to control subjects, showed a global (p = 0.002) and regional (p < or = 0.001) hypometabolism of glucose which normalized with weight gain. In relative values, no global difference could be assessed between underweight anorectic patients and controls but a trend can, nevertheless, be observed toward parietal and superior frontal cortex hypometabolism associated with a relative hypermetabolism in the caudate nuclei and in the inferior frontal cortex. After weight gain, all regions normalized for absolute and relative values, although a trend appears toward relative parietal hypometabolism and inferior frontal cortex hypermetabolism in weight gain anorectic patients. Absolute brain glucose hypometabolism might result from neuroendocrinological or morphological aspects of anorexia nervosa or might be the expression of altered neurotransmission following deficient nutritional state. As some differences exists in relative values in underweight patients and tend to persist in weight gain states, this could support a potential abnormal cerebral functioning, a different reaction to starvation within several regions of the brain or different restoration rates according to the region.
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PMID:Brain hypometabolism of glucose in anorexia nervosa: normalization after weight gain. 889 69

Although excessive physical activity and obsessive compulsiveness are both prevalent in anorexia nervosa (AN), to date, the association between these two factors has not been systematically investigated. The aim of the present study was to investigate the relationship between obsessive compulsiveness and both behavioral and psychological aspects of exercise in women with AN, and to compare them to a nonclinical sample of females classified as either moderate or high-level exercisers. Results indicated that obsessive compulsiveness, weight preoccupation, and pathological aspects of exercise were significantly related to the level of physical activity among the eating disorder patients. For the high-level exercisers, only obsessive compulsiveness was significantly related to the amount of physical activity. The findings are discussed in terms of a model in which physical activity, starvation, and obsessive compulsiveness are reciprocally and dynamically related, with each factor creating a destructive bidirectional loop that is resistant to change and difficult to break. We propose that this self-perpetuating loop may be a significant influence in the development and maintenance of eating disorders in a certain subgroup of women.
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PMID:Obsessive compulsiveness and physical activity in anorexia nervosa and high-level exercising. 892 6

We investigated the effects of malnutrition and refeeding on albumin distribution and metabolism in patients undergoing treatment for anorexia nervosa. Using autologous 125I-labelled albumin, we measured the fractional catabolic rate and calculated the relative sizes of the plasma and extravascular albumin pools in 6 female anorexia nervosa subjects and 6 matched controls. We were unable to demonstrate any differences in either the catabolic rate of albumin (fractional or absolute) or in serum albumin concentration between anorexia nervosa and control subjects. There was a large expansion of the extravascular albumin pool in the anorexia nervosa subjects--36% when expressed in relation to body weight. We conclude that, at the time of study, there were no effects of anorexia nervosa on albumin catabolism in these subjects. However, the condition and its treatment are associated with a significant relative expansion of the extravascular albumin pool. This contrasts to some extent with previous work, which suggested that in protein depletion the plasma albumin pool is maintained at the expense of the extravascular albumin pool. The expansion of the extravascular albumin pool is possibly related to the relative excess of interstitial fluid seen in starvation and in the initial phases of refeeding.
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PMID:Serum albumin distribution in early treated anorexia nervosa. 893 98

Anorexia nervosa is associated with multiple endocrine abnormalities. Hypothalamic neuropeptides and monoamines are involved in the regulation of human appetite, and they are changed in several ways in anorexia nervosa. But it remains to be clarified whether these alterations are secondary or etiologic. Feeding behaviour in anorexia nervosa is characterised by a strong ambivalence and not by loss of appetite. Hypothalamic amenorrhea is a diagnostic criterion, and is not only secondary as it often precedes the weight loss and persists for a long time after weight and motor activity have returned to normal. Hypersecretion of corticotropin releasing hormone seems to be secondary to starvation, but at the same time it may keep up and intensify the anorexia, physical hyperactivity and amenorrhea. Low production of insulinlike growth factor-I and high growth hormone secretion reflects the nutritional deprivation. In conclusion most of the neuroendocrine abnormalities are secondary to weight loss, but some of them seem to participate in a circulus vitiosus and maintain the emaciated state.
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PMID:[Neuroendocrine disorders in anorexia nervosa--primary or secondary?]. 899 10

Several studies have addressed the question of the effects of starvation on immune function and changes in lymphocyte subsets. Patients with anorexia nervosa are severely malnourished, but there have been few studies of immune parameters in this group. For this reason, phenotypic markers of T cell function and activation were studied in 20 severely underweight patients with anorexia nervosa and again after a period of refeeding. The most significant finding was a reduction in the percentage and absolute number of CD8+ T cells in patients with anorexia, the result of a marked reduction in memory (CD45RO+RA-) CD8 cells. A tendency for recovery in numbers of this subset was seen after refeeding. A decreased memory:maive cell ratio was also seen among CD4 cells, but was less marked. Subtle abnormalities in activated CD4 and CD8 cells were also found in the patient group at the initial sampling, but did not follow any clear pattern. These findings indicate that starvation in anorexic patients is accompanied by a large change in memory CD8 T cells. It may be speculated that this relates to the perceived lack of symptomatic common viral infections in underweight anorexic patients and their return with the recovery of weight.
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PMID:T lymphocyte subpopulations in anorexia nervosa and refeeding. 932 79

The endogenous plasma alkaloids codeine and morphine were shown to be elevated in patients with anorexia nervosa and bulimia nervosa compared to control subjects. The role of these opioids in the pathophysiology of these eating disorders is discussed in relation to an auto-addiction opioid model. This model proposes that endogenous opioids are released during an initial period of dieting and reinforce a state of starvation dependence [1,2].
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PMID:Endogenous codeine and morphine in anorexia and bulimia nervosa. 915 Apr 13

The effect of starvation-related malnutrition on muscle performance and on the energy cost of exercise remains unknown, as does the timing of improvement by refeeding. Indeed, in most diseases that induce malnutrition, muscle dysfunction is worsened by an inflammatory process. Thus, physical performance and the energy cost of exercise were studied in 15 semistarvated malnourished anorexia nervosa (AN) patients during exercise on an ergometric bicycle (3-min steps of 30 W) before and after 8, 30, and 45 d of refeeding. Results were compared with those of 15 normal-weight healthy subjects matched for age, sex, and physical activity. Before refeeding, the workload reached during the exercise was 49% lower in AN patients than in control subjects (P < 0.01). It was correlated with body weight, fat-free mass, and leg muscle circumference (P < 0.002). The performance improved dramatically during refeeding (P < 0.03), reaching normal values after 45 d of refeeding, despite fat-free mass and leg muscle circumference values that were still 20% lower in AN patients than in control subjects (P < 0.01). At this time, the exercise-related VO2 remained unchanged, being approximately 25% lower than that of the control subjects when corrected for muscle mass differences (P < 0.03). In conclusion, in AN patients muscle performance was restored by refeeding long before the patients achieved normal nutritional status. The economic cost of physical activity for these malnourished patients allows them to maintain a relatively high level of physical activity. This relative overactivity has two goals in AN: it reinforces anorexia and contributes to the excess of energy expenditure needed for weight loss.
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PMID:Refeeding improves muscle performance without normalization of muscle mass and oxygen consumption in anorexia nervosa patients. 917 82

Complement plays important roles in host immune defences, and recent studies suggest that adipose tissue is an important site of production for some complement proteins. Starvation has been associated with low complement levels, but studied populations have usually had concomitant opportunistic infections or other conditions which might affect complement levels. To determine the impact of body weight and changes in body weight on serum complement, we investigated levels of complement proteins in otherwise healthy patients with a wide range of body weights, including patients with anorexia nervosa before and after treatment, obese dieters before and after weight loss, and normal weight controls. We found that complement proteins of the alternative pathway (C3, B, and D), alternative pathway haemolytic activity (AP50) and the inhibitors H and I were low in starving anorectics and normalized with weight gain. C3a levels were comparable in anorectics at low weight and after weight gain, indicating that low serum complement levels were attributable to hypoproduction and not complement cascade activation with consumption. Further, levels of C3, B, AP50, H and I, but not D, were higher than controls in obese patients and decreased toward normal after weight loss. Overall, percentage of ideal body weight, changes in body weight, and serum transferrin were each highly correlated with serum levels of complement proteins. We conclude that levels of alternative pathway complement components are determined in part by factors that influence body weight and by weight changes, possibly due to changes in production in adipose tissue or at other sites.
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PMID:Effect of body weight and caloric restriction on serum complement proteins, including Factor D/adipsin: studies in anorexia nervosa and obesity. 918


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