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

A case of a patient with hyperinsulinism due to insulinoma associated with neurological and psychiatric disturbances including EEG alterations is reported. The hunger test as well as the i.v. tolbutamid test proved to be of diagnostic importance. In addition, the electroencephalographic studies combined with blood sugar analyses before and after 50 g glucose, orally, showed a reversibility of the EEG alterations together with normalization of the blood surgar levels. These results point to the possibility of differentiating biochemical from structural cerebral lesions associated with hyperinsulinism.
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PMID:[Hyperinsulinism. Neurological and psychiatric aspects (author's transl)]. 5 30

Varied clinical observations of the presence of either hunger or anorexia during intragastric or intravenous alimentation have led to the current experiments. Nine rhesus monkeys (Macaca mulatta) were involved in studies of the long-term effects of enteral and parenteral nutrition on appetite as assessed by feeding behavior and gastric motility. The monkeys received either intragastric infusions of glucose or a complete liquid diet, or intravenous infusions of glucose or glucose/amino acid solutions. Oral intake was accurately adjusted to account for the calories administered by the intragastric route. Oral intake was also reduced in a calorically equivalent amount to account for the calories received during intravenous glucose. When glucose/amino acid solutions were administered parenterally, adjustments were less accurate, with resultant overeating and weight gain in some monkeys during parenteral nutrition, followed by prolonged suppression of appetite after cessation of the infusions. Further studies of the effects of varied compositions of parenteral nutrition, and varied methods of weaning from infusions, are indicated.
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PMID:Effects of enteral and parenteral nutrition on appetite in monkeys. 9 52

1. Glucokinase is one of four glucose phosphorylating enzymes present in rat liver. Its distinctive features are a high K-m for glucose (high-K-m isozyme) and a rather narrow substrate specificity. In contrast, the other three enzymes, collectively called hexokinases or low-K-m isozymes, exhibit low K-m values for glucose and a wider substrate specificity. 2. Glucokinase is present in the liver os mammals (with some exceptions), amphibians and lower reptiles; It is absent from higher reptiles and birds. The presence or absence of glucokinase may represent an evolutionary adaptation to feeding habits and other physiological peculiarities. Differences in the immunological behavior and in the kinetic parameters of glucokinases from different taxa suggest the operation of divergent evolution. 3. The levels of glucokinase in rat liver depend strictly on the supply of carbohydrate in the diet. Glycogen phosphorylase and glycogen synthetase behave similarly, whereas other carbohydrate-metabolizing enzymes depend on the provision of either protein or protein plus carbohydrate. Glucokinase decays with a half-life of 33 hr when rats are starved or fed a carbohydrate-free diet, and is induced by the administration of glucose. The adaptive character is not exhibited by all mammals, indicating evolutionary discrimination within the same class and even within the same single order Rodentia. Enzyme adaptation in the liver may partially explain the condition known as 'hunger diabetes'. 4. The endocrine system plays a paramount role in glucokinase adaptation, since insulin is essential for glucose-dependent glucokinase induction and, on the other hand, glucagon, catecholamines and cyclic AMP prevent the induction. Glucocorticoids and some pituitary hormones modulate the rate of induction. The mechanisms underlying the hormonal regulation of glucokinase levels are not well known. 5. The variations in liver glucokinase correspond to changes in the amount of enzyme protein as assessed by immunochemical titration. This fact agrees with the effects of inhibitors of protein synthesis on glucokinase induction. 6. An antiserum against rat glucokinase reacts with the enzyme from mammals and turtles but not with the amphibian enzyme. It does not react with low-K-m hexokinases from different sources. 7. The saturation function for glucose is sigmoidal in mammalian and amphibian glucokinases but not in glucokinase from lower reptiles. The Hill's coefficient is very constant with values about 1.6. The K0.5 (concentration for half saturation) values in the different species studied vary between 1.5 and 8 mM. These kinetic parameters may be considered as another adaptive feature aimed to give maximal efficiency to the liver uptake of glucose at the changeable concentrations in the blood resulting from variations in the amount of dietary glucose.
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PMID:Adaptive character of liver glucokinase. 16 20

Lipoatrophic diabetes has been produced in rabbits by injection of a fraction prepared from the urine from patients with congenital generalized lipodystrophy. Both these conditions are considered to be hypothalamic syndromes. The animals, and a patient with congenital generalized lipodystrophy and latent diabetes were treated with the dopamine receptor blocker, pimozide, for 4 and 17 months, respectively. The results were discouraging even though the patient got a daily dose of 16 mg pimozide. Fenfluramine has a lowering effect on brain serotonin, and peripheral effects on glucose and triglyceride metabolism. This drug improved the general condition of the rabbits with lipoatrophic diabetes, as well as that of the patient with congenital generalized lipodystrophy. The rabbits became normoglycaemic and insulin sensitive. In the patient a normalization of the urinary excretion of the serotonin metabolite 5-OH-indole acetic acid was observed. His voracious hunger and profuse perspiration were reduced, the hyperkeratotic layer of the skin peeled off, and the pigmentations of the skin decreased. There was observed an improvement of ALAT and ASAT, normalization of the fasting blood glucose, and increased sensitivity to exogenous insulin. After 11 months of 200 mg fenfluramine daily addtitional administration of 2 g clofibrate per day produced normalization of the serum triglyceride concentration and a marked reduction of the resistance to insulin. Three more patients with congenital generalized lipodystriphy, two of whom have manifest diabetes, have now started treatment with fenfluramine and are improving. The rabbits got relapse of their lipoatrophic diabetes when the fenfluramine treatment was stopped. It is suggested that a disturbance in the serotonin metabolism of the central nervous system may be of pathogenetic importance in congenital generalized lipodystrophy.
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PMID:Congenital generalized lipodystrophy and experimental lipoatrophic diabetes in rabbits treated successfully with fenfluramine. 57 33

Congenital generalized lipodystrophy is considered to be a diencephalic syndrome with disturbance of hypothalamic transmitters. After puberty and arrest of growth the patients develop a serious untreatable diabetes mellitus. One of our patients, a girl 15 years of age, developed a lipodystrophic diabetes with fasting blood glucose levels above 300 mg/100 ml, increased serum insulin with insulin resistance, and hyperlipidaemia. Daily administration of fenfluramine gave a dramatic improvement. The voracious hunger and profuse perspiration were reduced, the patient's serum lipids became normal, her blood glucose fell, and her sensitivity to exogenous insulin increased. A normalization of the urinary excretion of the serotonin metabolite, 5-OH-indole acetic acid, was observed.
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PMID:Lipodystrophic diabetes treated with fenfluramine. 61 40

1. In anaesthetized cats, the unitary activity of seventy-eight sensory vagal neurones was recorded in nodose ganglia by means of extracellular glass microelectrodes. 2. These neurones were stimulated by perfusion of the small intestine (duodenum and first part of jejunum) with glucose or other different carbohydrates at concentrations of 1--20 g/l. (i.e. 55--1100 m-osmole/l.). 3. The neurones were slowly adapting to stimulation and their discharge frequency was always low (1--30 Hz). 4. The activity of these neurones depended on the particular carbohydrate used and on its concentration: the discharge frequency generally increased when the concentration rose. 5. The neurones were of the C type (conduction velocities: 0.8--1.4 m/sec; mean, 1.1 m/sec). 6. In contrast with the known neurones connected to the gastro-intestinal tension receptors, they were not obviously activated by intestinal contractions or distensions. 7. In the same way, the stimuli which produced the response of other known endings, i.e. the mucosal receptors, were not effective; these stimuli included in particular stroking of the mucosa, over-distension of the bowel, intestinal perfusion with alkaline or acid solutions. On the other hand, the use of substances other than glucose (KCl and NaCl of the same osmolarity) showed that the osmotic pressure was not directly related to the receptor activation. 8. Therefore it is proposed to call the endings corresponding to these neurones 'glucoreceptors'. 9. The effect of glycaemia and intestinal motility were also studied. These variables acted presumably by changing the intestinal absorption rate. 10. The functional characteristics of the glucoreceptors (in particular the short latency of their response) strongly suggested that they were located close to the intestinal epithelium. 11. An ultrastructural study was performed in an attempt to identify the histological site of the receptors. Many non-medullated fibres were observed in the villi, especially beneath the epithelial layer. They gave complex branchings with abundant swellings. Some of them, at least, belonged to the vagal sensory component, because they were less numerous after unilateral selective sensory vagotomy. Therefore these complex endings could serve as the vagal glucoreceptors. 12. The roles of vagal intestinal glucoreceptors are discussed. Their functional characteristics as well as the clinical and experimental data suggest that they may be involved in the regulation of different types of alimentary behaviour (hunger, thirst, alliesthesia) and energy balance.
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PMID:Vagal glucoreceptors in the small intestine of the cat. 72 54

Insulin, a primary metabolic hormone, plays a dominant role in the regulation of food intake. An increase in the level of circulating insulin produced by its prandial release from endogenous stores is associated with the state of satiety. On the other hand, an increase in the insulin level produced by its exogenous administration, as well as by its excessive and prolonged release in certain pathological states or during the period of nocturnal overeating, paradoxically gives rise to the sensation of hunger. This differential effect of endogenous and exogenous insulin is analyzed in view of experimental and clinical evidence concerning the principal mechanisms in the regulation of food intake. These include the interrelation of central and peripheral glucosensitive systems, the involvement of the enteroinsular axis, and the effects on these regulatory mechanisms of the physiological state produced by changes in circulating insulin levels. The essential role of the vagus nerve in mediating the hunger and satiety induced by the lack of excess of glucose for cellular oxidation places the short-term glucostatic control in the periphery where the insulin is primarily acting. A unifying hypothesis concerning the role of insulin in the regulation of good intake is proposed and its clinical implications suggested.
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PMID:The role of insulin in the glucostatic control of food intake. 82 7

In addition to established gastrointestinal hormones--secretin, cholecystokinin-pancreozymin (CCK-PZ), gastrin, and glucagon---some 30 polypeptides with gastrointestinal actions can be listed. New aspects of these substances include the following: Gastrin and vasoactive intestinal peptide (VIP) can be also encountered in the central nervous system and may act as transmitters. CCK-PZ-serum concentrations are found markedly elevated in patients with exocrine pancreatic insufficiency; this may provide the opportunity to establish a realtively simple screening test. Moreover, there is evidence that serum-CCK-PZ levels serve as satiety signal. Secretin secretion is said to be enhanced in hunger and then to act as a lipolytic hormone. In addition to enteroglucagon, a gastrintestinal peptide identical to pancreatic glucagon has been detected. Gastric inhibitory polypeptide (GIP) inhibits gastric secretion and motility (enterogastrone activity) and together with glucose it stimulates insulin release (incretin activity). Motilin increases lower esophageal sphincter pressure, enhances gastric pepsin secretion and slows down gastric evacuation. Serum levels of pancreatic polypeptide may be found elevated as a diagnostic index in patients with endocrine peptide tumors of the pancreas. Recently, the potential importance of local (paracrine) actions of gastrointestinal polypeptides has been amphasized. Predominantly paracrine activity is exhibited by some prototype hormones, e.g. somatostatin, substance P, bombesian, and the non-polypeptide compounds, prostaglandins.
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PMID:[New views on gastrointestinal hormones]. 85 99

Intracellular glucopenia induced by 2-deoxy-D-glucose (2DG) administration in man produces increased hunger ratings and magnitude estimates of pleasantness for sucrose solutions. Augmented food intake substantiates these changes in affective behavior and relieves experimentally induced hunger. Intracellular glucopenia activates counterregulatory mechanisms to raise plasma glucose concentrations. Inducing hunger experimentally with 2DG provides a useful method for studying appetitive behavior in humans. The neurohumoral control of pituitary hormone release and other hypothalamic functions may be examined after 2DG infusion.
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PMID:Hunger in humans induced by 2-deoxy-D-glucose: glucoprivic control of taste preference and food intake. 92 88

Karyometric measurements in rats which for 30 days had received a glucose diet or a glucose diet supplemented with thiamine showed the following decrease in nuclear size in contrast to no treated controls. (see article) In both experimental groups there was a 30% loss of weight during the course of the experiment. The different decreases in nuclear volume in the examined organs cannot be explained only by a relative state of hunger. The very large decrease in activity in the fasciculated zone of the adrenal cortex is explained as an adaptation mechanism favouring glucose oxidation by insulin, and the relative increase in activity in the adrenal medulla as an adaptation mechanism to accomplish an elevated lipolysis.
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PMID:[Karyometric studies of the pancreas and adrenal glands of the albino-rat fed an unbalanced glucose diet or a glucose diet supplemented with thiamine]. 109 41


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