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

Sodium excretion and the blood levels of aldosterone, renin, atrial natriuretic peptide (ANP), and insulin were investigated in 9 women with obesity of alimentary-constitutional type during hunger therapy and resumed nutrition. It has been assumed that restricted sodium excretion with the kidneys during fasting is mainly caused by activation of the renin-angiotensin-aldosterone system, with ANP contributing to it, insulin not playing the major role in this process.
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PMID:[Hormonal regulation of sodium excretion by the kidneys during hunger therapy of obese patients]. 138 80

Drinking response to the intravenous administration of insulin (0.1 U/kg) was studied in 15 volunteers (eight males and seven females). Water intake was significantly higher after insulin than after saline administration during the 90-min period studied. Plasma glucose decreased significantly in individuals receiving insulin and the time of the maximum decrease (30 min) was concurrent with the beginning of water intake. Haematocrit values in the insulin-treated group were also significantly higher at that time. Plasma renin activity (PRA) after insulin administration was higher than under basal conditions or after saline injection. On the other hand, psychological responses indicated that insulin probably elicits thirst prior to the hunger which appears with hypoglycaemia. A possible role of endogenous insulin in meal-related thirst is hypothesized.
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PMID:Insulin stimulation of water intake in humans. 226 41

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

Detailed endocrine studies were carried out in 95 hospitalized obese patients during their treatment with diet and the tricyclic anoretic mazindol. The results obtained after 1 week or more of mazindol (2 mg or occasionally 4 mg/day) administration were compared with the results after placebo and with the initial pre-treatment values. There were no significant changes in the following parameters: FSH, LH, testosterone, renin, angiotensin II, growth hormone (GH) levels during insulin tolerance tests (ITT), 131I uptake, basal metabolic rate, Achilles tendon reflexes, T3 RIA, rT3 RIA, 17-ketosteroids and 17-ketogenic steroids in urine, both basal and after stimulation with ACTH and metyrapone. Blood glucose and plasma immunoreactive insulin (IRI) levels during oral glucose tolerance tests decreased during mazindol administration, IRI levels were significantly lower during ITTs after mazindol. T4 RIA serum levels increased significantly after mazindol. When mazindol was administered, GH levels increased somewhat in some obese patients during ITTs, while T3 RIA and rT3 RIA decreased in some patients. Mazindol has not only hunger (appetite) suppressing properties, but it probably affects the metabolism of energy substrates as well. The drug was well tolerated and there were no pathological findings in routine laboratory examinations during a long-term study with mazindol (non-stop treatment for 6 months).
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PMID:Endocrine studies with mazindol in obese patients. 677 43

The progression of animal life from the paleozoic ocean to rivers and diverse econiches on the planet's surface, as well as the subsequent reinvasion of the ocean, involved many different stresses on ionic pattern, osmotic pressure, and volume of the extracellular fluid bathing body cells. The relatively constant ionic pattern of vertebrates reflects a genetic "set" of many regulatory mechanisms--particularly renal regulation. Renal regulation of ionic pattern when loss of fluid from the body is disproportionate relative to the extracellular fluid composition (e.g., gastric juice with vomiting and pancreatic secretion with diarrhea) makes manifest that a mechanism to produce a biologically relatively inactive extracellular anion HCO3- exists, whereas no comparable mechanism to produce a biologically inactive cation has evolved. Life in the ocean, which has three times the sodium concentration of extracellular fluid, involves quite different osmoregulatory stress to that in freshwater. Terrestrial life involves risk of desiccation and, in large areas of the planet, salt deficiency. Mechanisms integrated in the hypothalamus (the evolutionary ancient midbrain) control water retention and facilitate excretion of sodium, and also control the secretion of renin by the kidney. Over and above the multifactorial processes of excretion, hypothalamic sensors reacting to sodium concentration, as well as circumventricular organs sensors reacting to osmotic pressure and angiotensin II, subserve genesis of sodium hunger and thirst. These behaviors spectacularly augment the adaptive capacities of animals. Instinct (genotypic memory) and learning (phenotypic memory) are melded to give specific behavior apt to the metabolic status of the animal. The sensations, compelling emotions, and intentions generated by these vegetative systems focus the issue of the phylogenetic emergence of consciousness and whether primal awareness initially came from the interoreceptors and vegetative systems rather than the distance receptors.
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PMID:Hypothalamic integration of body fluid regulation. 869 5

Salt hunger is the behaviour of an animal suffering sodium deficiency. It is characterised by an increased motivation to seek and ingest sodium, and the ability to distinguish between sodium and other salts. Here I review the development of salt hunger in the rat. Salt hunger develops rapidly between birth and weaning. It can first be demonstrated 72 h postnatally when an intracerebroventricular injection of renin elicits greater swallowing of NaCl solution than water and greater mouthing of solid fragments of NaCl than of an artificial sweetener. However, sodium deficit per se cannot arouse the hunger at this age, and first elicits increased intake of NaCl only at 12 days-of-age. The next landmark is at 17 days-of-age when the hormonal synergy of aldosterone and central angiotensin II first elicits salt hunger, as it does in the adult. The specificity of the hunger for the sodium ion also develops postnatally: the 72 h-old sodium-hungry neonate does not distinguish between NaCl and other mono- and di-valent chloride salts but, increasingly during development, the sodium hungry pup distinguishes salts and by weaning age NaCl is clearly preferred to other salts almost as it is in adults. Early development may also be a sensitive period for determining lifelong preferences, and indeed, acute perinatal sodium depletion induces a lifelong enhancement of salt intake. Taken together, these findings demonstrate how a behaviour develops precociously and how, when the behaviour becomes important at weaning, the rat pup is competent to meet its sodium requirements, and may be adapted to anticipate sodium deficit.
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PMID:The ontogeny of salt hunger in the rat. 1039 57

Angiotensinogen, the precursor molecule of the peptides angiotensin I, II, and III, is synthesized in the brain and the liver. Evidence is reviewed that angiotensin II, and possibly angiotensin III, that are generated within the brain act within neural circuits of the central nervous system to regulate body fluid balance. Immunohistochemical studies in the rat brain have provided evidence of angiotensin-containing neurons, especially in the hypothalamic paraventricular nucleus, subfornical organ, periventricular region, and nucleus of the solitary tract, as well as in extensive angiotensin-containing fiber pathways. Angiotensin immunoreactivity is observed by electron microscope in synaptic vesicles in several brain regions, the most prominent of these being the central nucleus of the amygdala. Neurons in many parts of the brain (lamina terminalis, paraventricular and parabrachial nuclei, ventrolateral medulla, and nucleus of the solitary tract) known to be involved in the regulation of body fluid homeostasis exhibit angiotensin receptors of the AT(1) subtype. Pharmacological studies in several species show that intracerebroventricular administration of AT(1) receptor antagonist drugs inhibit homeostatic responses to the central administration of hypertonic saline, intravenous infusion of the hormone relaxin, or thermal dehydration. Responses affected by centrally administered AT(1) antagonists are water drinking, vasopressin secretion, natriuresis, increased arterial pressure, reduced renal renin release, salt hunger, and thermoregulatory adjustments. We conclude that angiotensinergic neural pathways in the brain probably have an important homeostatic function, especially in regard to osmoregulation and thermoregulation, and the maintenance of arterial pressure.
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PMID:Brain angiotensin and body fluid homeostasis. 1149 52

Obesity is strongly associated with hypertension and cardiovascular disease. Several central and peripheral abnormalities that can explain the development or maintenance of high arterial pressure in obesity have been identified. These include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Obesity is also associated with endothelial dysfunction and renal functional abnormalities that may play a role in the development of hypertension. The continuing discovery of mechanisms regulating appetite and metabolism is likely to lead to new therapies for obesity-induced hypertension. Better understanding of leptin signaling in the hypothalamus and the mechanisms of leptin resistance should facilitate therapeutic approaches to reverse the phenomenon of selective leptin resistance. Other hunger and satiety signals such as ghrelin and peptide YY are potentially attractive therapeutic strategies for treatment of obesity and its complications. These recent discoveries should lead to novel strategies for treatment of obesity and hypertension.
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PMID:Obesity-associated hypertension: new insights into mechanisms. 1558 75