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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rates at which neurons synthesize such Group I neurotransmitters as serotonin, acetylcholine, and the catecholamines norepinephrine and dopamine depend physiologicall on the availability to them of the circulating precursors for these compounds (tryptophan, choline and tyrosine, respectively). The concentrations of precursor in the circulation and in neurons change rapidly after food consumption, depending upon what is eaten. Nutrient intake thus normally influences the synthesis of these neurotransmitters. Neurons that emit signals by releasing serotonin, acetylcholine, dopamine, or norepinephrine participate in the control of a number of bodily functions and behaviors (e.g., hunger, food choice, sleep, alertness, sensitivity to environmental stimuli and disease states). Dietary manipulations (or the consumption of individual nutrients) can thus be used as tools for the experimental analysis of functions mediated by monoaminergic or cholinergic neurons, and as adjuncts in the treatment of some diseases of these neurons. It is unclear "why" the evolutionary process should have "allowed" the neurotransmission mediated by acetylcholine or the monoamine transmitters to be influenced by the vagaries of food choice. One possible benefit that might accrue to the organism as a result of this dependency would be the use of cholinergic or monoaminergic neurons as "sensors", providing the brain with information about peripheral metabolic state. Thus carbohydrate consumption, which--by altering plasma amino acid levels accelerates brain serotonin synthesis--enhances the release of a transmitter (serotonin) that tends to diminish the animal's desire to consume carbohydrates.
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PMID:When--and why--should nutritional state control neurotransmitter synthesis? 3 79

The responses of thirteen patients with bulimia nervosa and sixteen controls matched for age and weight are described following the ingestion of a carbohydrate and a calorie-free placebo mixture in simulated binges. Psychological, hormonal and biochemical parameters were measured before and at 15 minute intervals for two hours after the simulated binge. At baseline, the bulimics were clearly more symptomatic than the controls. The control population showed a specific satiating effect of carbohydrate upon hunger ratings. Bulimic patients responded differently showing a blunting of the normal sensation of hunger and an enhanced rating for nausea. Prolactin, growth hormone (GH) and cortisol failed to show a carbohydrate-mediated stimulation in either population. The bulimic patients showed a different pattern of GH release, but this was independent of the challenge condition. Large neutral amino acid (LNAA) levels fell following carbohydrate ingestion, but produced an increase of up to 20% in the tryptophan: LNAA ratio in both bulimic patients and the control group. Thus, while this increase in tryptophan availability failed to provoke hormone release, the time course of the carbohydrate specific effect on the sensations of hunger and nausea is compatible with a mechanism based on increased tryptophan availability. The confusion of satiety with nausea may provide a useful focus for the future treatment of patients with bulimia nervosa.
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PMID:Psychological, hormonal and biochemical changes following carbohydrate bingeing: a placebo controlled study in bulimia nervosa and matched controls. 204 88

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

Evidence from published studies and clinical experience indicates that neuroleptic drugs, tricyclic and heterocyclic antidepressants, monoamine oxidase inhibitor antidepressants, and lithium all possess varying abilities to increase appetite, stimulate carbohydrate craving, and cause weight gain over prolonged periods of administration. Sedatives and benzodiazepine-type antianxiety drugs fail to stimulate appetite or induce weight gain, and it is unlikely that the sedative or calming effects of other psychotropic drugs contribute significantly to changes in appetite or weight. Studies of the endocrine and metabolic aspects of psychotropic drugs suggest that these mechanisms do not contribute significantly to explaining the observed effects on appetite or weight. Numerous studies indicate that a wide variety of compounds, including the serotonin precursor, tryptophan, the serotonin receptor stimulant, fenfluramine, and the serotonin reuptake inhibitor, fluoxetine, are all capable of decreasing carbohydrate hunger, reducing consumption of carbohydrate-rich foods, and inhibiting weight gain in humans and animals. Widely divergent psychotropic drugs produce antagonistic effects at serotonin receptor sites, and it is likely that this action contributes to their ability to stimulate appetite, carbohydrate craving, and weight gain. Those psychotropic drugs that inhibit serotonin reuptake mechanisms, increasing serotonin activity within the central nervous system, either fail to stimulate carbohydrate hunger and weight gain or are actually capable of decreasing carbohydrate craving and facilitating weight loss. Because many antidepressants, including trazodone and amitriptyline, the neuroleptic, chlorpromazine, and the mood stabilizer, lithium, may all, under some circumstances, inhibit serotonin reuptake mechanisms and may simultaneously block serotonin receptor sites, their effects on appetite and weight gain may represent a balance between serotonergic and antiserotonin activities. Monoamine oxidase inhibitors, which slow the metabolic degradation of monoamines, including serotonin and norepinephrine, allow for increased levels of these neurotransmitters within the brain. It is conceivable that the relative noradrenergic effect related to an amphetamine-like structure of tranylcypromine may explain its lesser ability to stimulate appetite and weight gain than the appetite and weight effects observed with phenelzine. Furthermore, the production of dry mouth and thirst by psychotropic drugs appears to contribute to weight gain, secondary to consumption of high-calorie beverages.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Induction of obesity by psychotropic drugs. 288 2

The consumption of a carbohydrate-rich, protein-poor meal or snack can increase the synthesis of the brain neurotransmitter serotonin; proteins block this effect. The mechanism of the rise in brain serotonin involves the secretion of insulin, and the decrease that the hormone produces in plasma levels of certain amino acids that compete with tryptophan, serotonin's precursor, for transport across the blood-brain barrier. The rise in serotonin can thus be produced by any carbohydrate that elicits insulin secretion, independent of its sweetness. Pharmacologic treatments that amplify serotonin-mediated neurotransmission can selectively decrease the consumption of carbohydrate (i.e., in relation to that of protein). A group of diseases seems to exist in which depressive symptoms are associated with "carbohydrate-craving", and the consumption of large quantities of carbohydrate-rich, protein-poor snacks. Patients describe positive subjective responses to the dietary carbohydrates which are unrelated to hunger. These responses may be mediated by the rise in brain serotonin.
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PMID:Do carbohydrates affect food intake via neurotransmitter activity? 290 17

Food intake regulation is influenced by serum amino acid (AA) ratios. The objectives of this study were to determine whether non-obese subjects with diabetes have normal serum AA ratios, and to see if AA ratios relate to perceived hunger. We therefore measured fasting serum AA in nine normal subjects on two occasions and 19 patients with diabetes on four occasions over a two month period. At the time of the blood samples, the subjects with diabetes were asked to rate how hungry they felt on a scale of -3 (very hungry) to +3 (very full). There were no significant differences between the mean AA ratios of normal and diabetic subjects. There was a positive correlation between reported hunger score and the ratio of serum tryptophan (TRP) to the sum of the concentrations of the other large neutral AA (LNAA) (r = 0.286, n = 78, p less than 0.05). The relationships between hunger and other AA ratios were not significant. Variations of the TRP/LNAA ratio within each subject did not relate to differences in hunger from day-to-day. However, there was a positive correlation between the mean TRP/LNAA ratio and mean hunger score of the different subjects (r = 0.495, n = 19, p less than 0.05). The relationships between TRP/LNAA ratio and body weight or hunger score were not significant. It is concluded that the serum AA ratios are normal in patients with diabetes. The data is consistent with the hypothesis that a low serum TRP/LNAA ratio causes increased feelings of hunger in different individuals.
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PMID:Relationship between fasting serum tryptophan/large neutral amino acid ratio and reported hunger in subjects with diabetes. 324 45

A specific hunger for carbohydrate-rich foods has been observed in animals and human beings and appears to be regulated by the brain neurotransmitter serotonin. Consumption of a carbohydrate-rich meal increases the synthesis and release of brain serotonin (by enhancing the brain uptake of its precursor, tryptophan). As a consequence of this increased release of serotonin, carbohydrate intake is decreased at the next meal. Consumption of protein does not increase brain serotonin levels or decrease carbohydrate intake. A subgroup of obese individuals who consume carbohydrate-rich snack foods at specific times of day or evening has been identified. Such individuals do not routinely snack on protein-rich foods, and their consumption of calories and nutrients at meals is not excessive. Evidence is presented that carbohydrate snacking seems to be related to a "need" to increase the level of brain serotonin; treatment with a drug, d-1 fenfluramine, that increases serotoninergic neurotransmission significantly decreases carbohydrate snack consumption. Weight loss among the population of carbohydrate cravers might be most successful if treatment includes either a diet or drugs that increase brain serotonin activity when the need to snack on carbohydrate is most likely to occur.
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PMID:The involvement of brain serotonin in excessive carbohydrate snacking by obese carbohydrate cravers. 638 75

Using an 11-item questionnaire and a double-blind experimental design, changes in mood, hunger and food preference after taking caffeine (100 mg), tryptophan (500 mg), tyrosine (500 mg) or placebo, were investigated in 60 volunteers. At the end of the study, volunteers also ranked the four treatments on a sedation/stimulation scale. Caffeine significantly increased scores for wakefulness, vigor, clarity of mind, energy, feeling full of ideas, feeling full of go and feeling efficient. Caffeine was also ranked as the most stimulating treatment (p less than 0.001). Tyrosine produced no changes, while tryptophan shifted mean scores towards somnolent and lethargic, and was ranked most sedating (p less than 0.05). None of the treatments changed hunger ratings or carbohydrate/protein preference.
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PMID:Diet-induced mood changes in normal populations. 676 31

The amino acid tryptophan (tryp) is a potent inhibitor of gastric emptying in both animals and humans. Animal studies suggest that this effect may be specific for the L-enantiomer. The effects of D- and L-tryptophan on gastric emptying, intragastric distribution and appetite in humans were evaluated. Ten volunteers ingested 300 mL of either L-tryp (50 mmol/L), D-tryp (50 mmol/L) or normal saline labelled with 99mTc sulfur colloid on three occasions, separated by between 3 and 7 days. Hunger and fullness were measured with a visual analogue scale at -2, 15, 30 and 60 min after ingestion of each drink. Saline emptied faster from the stomach than both L-tryp and D-tryp (P < 0.05) and D-tryp emptied faster than L-tryp (P < 0.005). Emptying from the proximal stomach was fastest for saline (P < 0.05) and faster for D-tryp than L-tryp (P < 0.005). Emptying from the distal stomach was faster for saline than both D- and L-tryp (P < 0.05). A reduction in hunger (P < 0.05) and a non-significant trend for an increase in fullness were observed after all three drinks. At 60 min, fullness was greater after L-tryp than after ingestion of D-tryp (P < 0.01). These observations indicate that the effect of tryptophan on gastric emptying in humans is stereospecific, consistent with the concept that stereospecific receptors for tryptophan exist in the human small intestine.
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PMID:Stereospecific effects of tryptophan on gastric emptying and hunger in humans. 786 13


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