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)

An account is given of the fundamental mechanisms concerned with the regulation of hunger and thirst, and of the physiological processes involved in the uptake of nutrients, water and electrolytes. Several reflex chains ensure that the organism does not take up too much water and also protect it from excessive loss of water and salt.
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PMID:[Physiological equilibration of water, electrolytes and nutrients]. 82 1

Polyuria in a herd of forty-five dairy cattle was the chief complaint in the first case. Polydipsia was the principle sign in a second case involving one dairy cow. Less conspicuous clinical findings included salt hunger, pica, weight loss and decreased milk production. Clinicopathologic investigation included monitoring the concentrations of sodium, potassium and chloiride in urine, parotid saliva and plasma. These analyses indicated a primary sodium deficiency which responded to sodium chloride ad libitum.
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PMID:Salt (sodium) deficiency in dairy cattle: polyuria and polydipsia as prominent clinical features. 123 30

Steroids (aldosterone and testosterone) and peptides of cerebral origin (angiotensin II and the tachykinins) control the salt intake of the rat. They arouse or suppress the behaviour and produce life-long enhancements of NaCl intake. Need-induced salt intake (salt appetite or salt hunger), which is the consequence of sodium deficiency, is aroused by a synergy within the brain of cerebral angiotensin II and aldosterone. And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Need-free salt intake, which occurs daily when the rat is in positive sodium balance, is inherently high in the rat and is organized in the perinatal period by aromatized testosterone which suppresses the intake of the male. It is also enhanced by prior activations of angiotensin II and aldosterone. Both need-induced and need-free salt intake are suppressed by intracranial tachykinins. Non-mammalian tachykinins (eledoisin, physalaemin, kassinin) are both antidipsogenic and antinatriorexigenic, but amino-senktide, an analogue of the mammalian tachykinin substance P with selective affinity for the NK 3 receptor, appears to be a selective antinatriorexigenic agent, and could provide a rational therapy for chronic overconsumption of salt.
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PMID:Control of salt intake by steroids and cerebral peptides. 163 90

Steroids (aldosterone and testosterone) and peptides of cerebral origin (angiotensin II and the tachykinins) control the salt intake of the rat. They arouse or suppress the behavior and they produce lifelong enhancements of NaCl intake. Need-induced salt intake (salt appetite or salt hunger), which is the consequence of sodium deficiency, is aroused by a synergy within the brain of cerebral angiotensin II and aldosterone. And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Need-free salt intake, which occurs daily when the rat is in positive sodium balance is also enhanced by prior activations of angiotensin II and aldosterone. Both need-induced and need-free salt intake are suppressed by intracranial tachykinins. Nonmammalian tachykinins (eledoisin, physalaemin, kassinin) are both antidipsogenic and antinatriorexigenic, but amino-senktide, an analog of the mammalian tachykinin substance P with selective affinity for the NK 3 receptor, appears to be a selective antinatriorexigenic agent, and could provide a rational therapy for chronic over-consumption of salt.
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PMID:Neurohormonal control of salt intake in the rat. 195 25

A human case infected with Stellantchasmus falcatus(Heterophyidae) is reported based on the adult worms collected after praziquantel treatment. The patient is a 33-year old male residing in Seoul. For several months he experienced vague abdominal discomfort and hunger pain. Praziquantel at a single dose of 600 mg was given followed by purgation with magnesium salt, and 17 adult S. falcatus specimens were collected from the diarrheal stools. He recalled he had eaten raw flesh of several kinds of brackish water fishes. This is the 4th human case of S. falcatus infection in Korea.
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PMID:A human case of Stellantchasmus falcatus infection. 248 40

Hypophysectomized and pituitary-intact rats were tested for their expression of salt hunger under a variety of experimental conditions. The results show that hypophysectomized rats ingest less salt in response to salt hunger induced by sodium depletion, captopril or angiotensin in comparison to pituitary-intact rats. In contrast, both groups ingest the same amount of salt in response to mineralocorticoid-induced salt hunger. While sodium excretion and plasma sodium levels were comparable in the two groups, the angiotensinogen mRNA was reduced by hypophysectomy in several limbic brain regions as well as in the liver. These results suggest that reduced salt intake in response to manipulations of the body sodium and renin-angiotensin system in hypophysectomized rats may result from decreased angiotensinogen mRNA levels.
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PMID:Expression of salt hunger in hypophysectomized rats. 268 42

Damage to the medial region of the amygdala abolished aldosterone-induced salt hunger in the rat. In contrast, the salt hungers that are induced by adrenalectomy or by acute sodium depletion are left intact by the same brain damage. We suggest (a) that we have identified part of the neural circuit by which aldosterone participates in the genesis of salt hunger in the intact, sodium-depleted rat and (b) that these results provide further evidence for the hypothesis that there are separate receptive systems in the brain for the participation of aldosterone and angiotensin in the arousal of salt hunger.
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PMID:A role for the medial region of the amygdala in mineralocorticoid-induced salt hunger. 292 71

We examined the interaction of the metabolic fuels, glucose and free fatty acids (FFA), in the control of food intake in Syrian hamsters. Hamsters were treated with a 2-deoxy-D-glucose (2DG) which inhibits glucose utilization, and methyl palmoxirate (MP), which inhibits fatty acid oxidation. The 2DG and MP, alone or in combination did not enhance food intake in hamsters fed a standard rodent chow diet. Determination of the circulating glucose, FFAs, and ketones confirmed that the drugs were having the intended metabolic effects. The 2DG caused marked hyperglycemia and decreased ketones consistent with an inhibition of glycolysis, and the MP caused increased FFAs and decreased ketones indicating inhibition of fatty acid oxidation. A third experiment examined the hamsters' willingness to ingest a diet made highly unpalatable with NaCl, another measure of hunger motivation. Although food-deprived hamsters ingested more of a salt-adulterated diet than did control animals, hamsters treated with MP and 2DG did not. These experiments provide further evidence that the control of food intake in Syrian hamsters is appreciably different than that of laboratory rats.
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PMID:Inhibition of fatty acid oxidation and glucose metabolism does not affect food intake or hunger motivation in Syrian hamsters. 323 26

Ingestive behavior in cattle differs from other species because of physiological mechanisms developed pari passu with fermentative digestion. The secondary refection of rumination allows remastication and reinsalivation of the large bulk of vegetable food ingested. The need to buffer acid products of cellulose digestion demands continuous high secretion of alkaline saliva. Nervous and hormonal stimuli emanating from the gastrointestinal tract evoke centrally controlled behavior of hunger and satiety. The four primary taste receptors occur in cattle but thresholds are low. Because of the low Na level in plants, cattle have developed the behavior of seeking salt by taste and smell. During Na deficiency it can be shown that cattle readily learn and develop memory, providing a powerful behavioral dimension in the search for food.
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PMID:Aspects of ingestive behavior in cattle. 639 76

There is evidence in the literature that has been taken to show that, unlike hunger and thirst, salt appetite cannot be satiated in the absence of salt taste stimulation. The present study showed that repletion of body sodium in the absence of taste stimulation, that is, by gavage, can diminish subsequent saline intake. The satiating effects of gavage versus drinking of saline were studied at various intervals after repletion. For the first few hours, gastric loading was constantly less satiating than was drinking. But as the interval between gavage and testing was lengthened beyond 4-8 hr, the satiating effect began to increase until by 16 hr it was equal to that of drinking. The specificity of the satiating effect of saline gavage as a function of time between treatment and testing was also studied. There appeared to be a transient nonspecific blocking effect of solutes on solute intake which had a duration of less than 30 min. The satiating effect of saline gavage became specific after that time. The experiment suggests that there are multiple factors involved in the satiation of salt appetite--a taste factor, a short-latency post ingestional factor, and a long-latency postingestional factor.
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PMID:Multiple factors in the satiation of salt appetite. 646 42


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