Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As endogenous opiates are known to be involved in regulation of appetite, an obese patient with panhypopituitarism and frequent episodes of ravenous hunger was treated with the oral opiate antagonist naltrexone for 13 months. This resulted in loss of body weight and attacks of severe hunger. The increased serum prolactin concentration and the dose of vasopressin required for substitution could be reduced. Long-term application of opiate antagonists may be useful in related cases.
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PMID:Long-term opiate receptor antagonism in a patient with panhypopituitarism: effects on appetite, prolactin and demand for vasopressin. 204 62

The secretion of prolactin and growth hormone (GH), together with subjective ratings of sedation and hunger, were determined in 13 in-patients with anorexia nervosa and 15 controls during the intravenous infusion of L-tryptophan (100 mg/kg). Prolactin responses were not different between groups but GH responses were markedly blunted in patients. In addition sedation responses in patients were attenuated compared with controls. Hunger ratings were reduced by the infusion in controls but were too variable to be interpreted in the patients. Plasma amino acid levels were also determined before and after infusion of L-tryptophan. Tryptophan levels were comparable in the two groups as were the levels of tyrosine, phenyl alanine, valine, leucine and iso-leucine. The results suggest that some aspects of 5-hydroxytryptamine function may be attenuated in anorexia nervosa. However, they undoubtedly contrast with the finding of enhanced hormonal responses in acute dieting and may be relevant to the interpretation of similar experiments in depressive illness.
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PMID:The neuroendocrine responses and psychological effects of infusion of L-tryptophan in anorexia nervosa. 259 82

It has been suggested that bingeing and vomiting behavior may be an attempt to suppress hunger or reduce dysphoria. Theoretically, such relationships could involve a mechanism whereby bingeing and vomiting change plasma amino acids which, in turn, enhance brain serotonin-mediated satiety and/or improvement in mood. This hypothesis is based on data showing that the intake of dietary carbohydrates increases the uptake of tryptophan (TRP), the precursor of serotonin, into the brain by increasing the plasma TRP ratio (the ratio of the plasma TRP concentration to the summed concentrations of other amino acids that compete with TRP for brain uptake). Plasma prolactin (PRL) release might reflect the activation of this system. We found that an increase in the TRP ratio during bingeing and vomiting was associated with satiety (i.e., cessation of bingeing and vomiting), but not change in mood. In other words, bulimic subjects who developed an increased plasma TRP ratio during bingeing and vomiting had fewer cycles of bingeing and vomiting and a greater increase in plasma PRL than did subjects who did not develop an increase in the plasma TRP ratio. This study raises the possibility that an increase in the TRP ratio may be associated with the termination of bingeing and vomiting, perhaps due to its effects on brain serotonin metabolism.
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PMID:Bingeing behavior and plasma amino acids: a possible involvement of brain serotonin in bulimia nervosa. 283 64

The present study was conducted to investigate the relationship of psychopathological, behavioral and neuroendocrinological variables to weight profiles in patients with anorexia nervosa. The subjects were 67 patients with anorexia nervosa (61 females, 6 males). Eighteen (27%) were found to have a diffuse organic brain syndrome. Symptoms of hysterical and depressive neurosis predominated among the female subjects and those of obsessive-compulsive neurosis among the male subjects. Obsessive-compulsive and depressive traits were seen more frequently in the subjects with organic brain syndrome (14 of 18) than in the other subjects. One third of the female subjects showed resistance during therapy. Neuroendocrinological investigations (LHRH and TRH tests) were carried out on 27 of the female subjects. The stimulation values for the hormones LH, FSH, TSH and prolactin showed a significant dependence on weight. The symptomatology found in the subjects with organic brain syndrome largely parallels that of the psycho-organic hunger syndrome described by Baeyer. Correlations were found between weight loss and both blood chemistry findings and changes in psychosocial behavior.
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PMID:[Anorexia-nervosa--psychopathologic findings in relation to body weight and neuroendocrinologic changes]. 393 81

Ten healthy male volunteers of normal weight received 30 mg of D-fenfluramine, a putative selective releaser of 5-hydroxytryptamine (5-HT), and placebo by mouth in balanced order at a 1 week interval after a light breakfast. Blood was taken for estimation of plasma cortisol and prolactin, and the patients completed self rating scales for stress and arousal and rated themselves on visual analogue scales for mood, hunger and alertness at appropriate time points from 30 min before to 300 min after drug/placebo ingestion. There were no statistically discernible effects of D-fenfluramine on either hormone measures or subjective ratings. The failure to find effects may be due to a too low dose of D-fenfluramine and/or a lower sensitivity to the drug in men compared with women. More information is required on the dose/response relationship and drug absorption especially after food. However, the findings cast doubt on results already obtained employing this dose of the drug in studies that have included male subjects. Furthermore, the interpretation of earlier studies with D,L-fenfluramine at a dose of 60 mg is also made more uncertain by the failure to confirm that the more selective D-isomer produces equivalent effects.
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PMID:Oral D-fenfluramine and neuroendocrine challenge: problems with the 30 mg dose in men. 820 Nov 26

The behavioural, cognitive and metabolic response to food intake was studied in 13 adults with the Prader-Willi syndrome (PWS) and compared to ten age-matched controls. Rates of eating were observed during one hour's access to food and feelings of hunger were assessed using a visual analogue scale. Blood was taken for estimation of glucose, insulin, cholecystokinin (CCK), prolactin, growth hormone (GH) and cortisol every 20 min for a total period of 100 min. Ten (76%) of the subjects with PWS ate steadily for the whole hour that food was available and on average consumed three times more calories than the control group. The median ratings for feelings of hunger in the PWS group changed in the expected direction but these changes were delayed compared to the control group and only reached the same level as the controls after the PWS subjects had eaten a significantly greater amount of food. In the PWS group, in contrast to the control group, feelings of hunger started to re-emerge shortly after food was removed. There were marked differences between individuals with PWS in the extent of the changes in serum prolactin levels. Increases in plasma glucose levels were inversely correlated with changes in hunger ratings in the PWS group, but not the control group. There was a significantly greater increase in serum CCK levels during the meal in the PWS group than in the control group indicating that in PWS failure of peripheral release of CCK in response to food intake was not the explanation for the impaired satiety response.
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PMID:Measurement of excessive appetite and metabolic changes in Prader-Willi syndrome. 822 Jun 55

We studied the effect of 2 weeks administration of the 5-HT2C receptor agonist, m-chlorophenylpiperazine (mCPP), on appetite and body weight in 18 moderately obese subjects in a double-blind, placebo-controlled trial, mCPP caused a small but significant (0.75 kg) reduction in body weight and in subjective ratings of hunger. Plasma prolactin was significantly elevated by the final dose of mCPP. Our data suggest that during 2 weeks treatment in humans, mCPP may continue to activate brain 5-HT2C receptors, and that this effect is associated with decreases in appetite and body weight.
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PMID:5-HT2C receptor activation decreases appetite and body weight in obese subjects. 936 39

Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. beta-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.
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PMID:Afferent signals regulating food intake. 1099 53

Ghrelin is a peptidic hormone composed of 28 aminoacid residues. It is produced by enteroendocrine cells of stomach and intestine. It is also produced in pancreas, kidney, placental tissue, thyroid gland, hypothalamus, and hypophysis. Gastrectomy leads to 65-80% decrease of plasma levels of ghrelin. In human organism, ghrelin stimulates secretion of growth hormone, prolactin, and ACTH. Ghrelin also has orexigenic activity (increases food intake), influences the sleep/wake cycle, gastric motility and secretion, cardiovascular functions, regulates endocrine function of pancreas and metabolism of glucose and shows an antiproliferative effect. Ghrelin is an important regulatory part of the homeostasis of the organism, and iterconnects neuroendocrine and metabolic response of the organism to starvation, and it is considered as a counterpart to leptin. Ghrelin was discovered by Japanese scientists in 1999 as a natural ligand of an "orphan" receptor GHS1a, which is specific for a group of synthetic peptides (growth hormone secretagogues--GHS) stimulating secretion of growth hormone. Plasma levels of ghrelin reflect short-time changes of food intake, as well as long-time changes of the nutritional state of the organism. Plasma levels of ghrelin are decreased after food intake and in obese humans, and they are increased during starvation and in patients with mental anorexia. Plasma levels of ghrelin in humans correlate negatively with body mass index, amount of body fat, size of adipocytes, and plasma levels of insulin, glucose, and leptin. Thus, ghrelin probably plays a role as a metabolic signal of hunger.
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PMID:[Ghrelin--structure, function and clinical applications]. 1570 43

Tskaltubo mineral waters have curative value due to radon in it. As biochemical data evidence the quantitative changes of amino acids in blood and disorder in deaminization of amino acids lead to disorder in ammonia utilization. As it is known from literature, increase of ammonia is the determining factor of rising of excitability, a headache, and etc. causing the increase of emotionality and activation of nervous system. Agitation of sympathetic system due to stress increases secretion of prolactin directly or via dopamine suppression. Consequently amount of ammonia is increased and optimal range of sympathetic system is changed; the impact on adrenal glands leads to the pathology of hypothalamus-hypophysis system - hyperprolactinemia, hyperinsulinemia, excitement of centre of hunger, obesity. Analysis of experimental data proves the blocking effect of radon treatment on the development of life style illnesses; which are connected with the reaction of reoxidation and lowering of the immune system.
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PMID:[Biochemical results of radon treatment]. 1726 97


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