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

An hyperglycaemic metabolic state disappeared and spontaneous hypoglycaemia occurred in a 58-year-old woman with non-insulin-dependent obese type II diabetes. Abnormal absence of the hunger response with provoked hypoglycaemia, increased serum insulin concentrations and reduced blood glucose/insulin ratio led to the diagnosis of pathological hyperinsulinism, which was found to be due to an insulinoma of the tail of the pancreas. After its excision the patient's carbohydrate metabolism returned to a mild type II diabetic state and there were no further hypoglycaemic attacks.
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PMID:[Hypoglycemia caused by insulinoma in diabetes mellitus]. 284 54

Results of a number of studies have suggested that hyperinsulinemia and resultant hypoglycemia are part of a sequence of responses that can lead to hunger and to sugar-induced hyperphagia. However, it is argued in the present paper that neither hyperinsulinemia, hypoglycemia, nor any other factor per se is solely responsible for the hyperphagic effect of sugar or any other feeding effect. Also, the present paper emphasizes the need for caution in attempting to evaluate the role of a given factor in sugar-induced hyperphagia, or any other feeding effect, by eliminating the factor of interest. I have reviewed evidence indicating that the elimination of preabsorptive insulin, which may mediate sugar-induced hyperphagia, actually potentiates other factors that may mediate the same effect.
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PMID:Sugar-induced hyperphagia: is hyperinsulinemia, hypoglycemia, or any other factor a "necessary" condition? 305 64

Plasma gastrin and gastric acid responses to intravenous injection of insulin (0.2 IU/kg) were measured in 8 patients with Chagas' disease, which is known to be associated with extensive reduction of the intramural neurons of the digestive tract, and in 6 control subjects. All subjects developed hunger, sweating and tachycardia, and exhibited less than 50 mg/dl venous blood glucose. Plasma gastrin responses in Chagas' disease patients (median: 3.60 nmol L-1 min-1; range: 1:12 to 10.60 nmol L-1 min-1) were significantly higher than for control subjects (median: 0.52 nmol L-1 min-1; range: 0.25 to 1.09 nmol L-1 min-1). Gastric acid output was significantly lower in Chagas' disease patients (median: 3.5 mmol/h; range: 2.1 to 13.6 mmol/h) than in controls (median: 30.3 mmol/h; range: 7.3 to 38.2 mmol/h). These data show that chagasic patients have abnormally high gastrin release and low gastric acid secretion in response to insulin, and thus indicate that loss of intrinsic innervation of the stomach does not abolish the gastrin response to insulin hypoglycemia.
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PMID:Plasma gastrin and gastric acid responses to insulin hypoglycemia in Chagas' disease. 393 4

1. Aggressive behaviour was elicited in rats that had been deprived of food for 20 h daily (starved), by chronic administration of Cannabis sativa extract or (-)-Delta(9)-trans-tetrahydrocannabinol.2. The influence of intraperitoneal (i.p.) or oral glucose administration, cold environment, acidosis, and corn, and protein-free diets on this aggressiveness was studied.3. Intraperitoneal injections of glucose (100-1,600 mg/kg) did not alter the aggressiveness induced by marihuana in starved rats; glucose given orally, however, blocked this behaviour.4. Low temperature (14 degrees C) strongly potentiated the aggressive behaviour induced by marihuana in the starved rats.5. Lactic acid in doses capable of potentiating thiopental anaesthesia, failed to alter the marihuana-aggressiveness of starved rats or to facilitate this effect of marihuana in rats fed ad libitum. The same negative results were obtained with ammonium chloride.6. In rats fed ad libitum with protein-free or corn diets, marihuana administered chronically did not elicit aggressive behaviour. However, aggressiveness appeared when rats were fed for only 2 h daily on those diets.7. The results suggest that the stress of hunger (and not hypoglycaemia, acidosis or lack of specific nutrients due to starvation) is the factor that facilitates the development of aggressive behaviour by chronic administration of marihuana.
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PMID:Factors influencing the aggressiveness elicited by marihuana in food-deprived rats. 506 30

Animal experiments and clinical observations have demonstrated significant effects of vagotomy on body weight. Weight loss or inability to regain are partly due to impaired motility and secretomotor activity of the vagus nerve causing disturbances in digestion which, however, are not sufficient to explain most of the weight deficit after vagotomy in animals or morbidly obese patients. The body weight deficit is also due to reduced caloric intake with changes in the quantity and quality of food and liquid intake, the latter accounting for more than one-third of the total reduction in caloric intake. Obese patients have consistent decreases in hunger ratings after vagotomy and also reveal changed hedonic ratings and estimations of taste intensity. Validation of vagotomy studies requires tests of vagal integrity to confirm the completeness of the surgery and rule out regeneration of nerve tissue or recruitment of function. Tests of completeness of vagotomy are difficult to perform and evaluate in morbidly obese patients due to insulin resistance. The finding of an inadequate gastric acid response to insulin hypoglycemia implies a defect hypothalamic response to hypoglycemic stress in these patients. A new postoperative test of completeness of vagotomy based on disrupted drinking after intravenous hypertonic saline challenge is introduced as an attractive alternative to the potentially hazardous insulin test.
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PMID:Behavioral effects of vagotomy in humans. 636 99

The present study deals with the question as to what extent the sympathetically innervated rat pineal gland is affected by a number of short-term exogenous stimuli given during day-time, as assessed by measuring pineal serotonin-N-acetyltransferase activity (NAT) which is directly proportional to melatonin formation. In male Sprague-Dawley rats kept under LD 12:12 pineal NAT was statistically significantly depressed by physical immobilization for 2 hours, swimming for 15 min in water of 10 and 30 degrees C, exposure for 2 hours to cold (5 degrees C) or heat (40 degrees C), noise (90 db) for 2 hours and hunger for 17 hours. An increase in NAT was noted after swimming for 15 min in water of 20 degrees C. No effect was detectable after 17 hours of thirst or hunger combined with thirst and in one of 2 experiments involving exposure to heat (40 degrees C, 2 hours) and insulin-induced hypoglycemia. In animals kept under continuous illumination for 48 hours, immobilization resulted in a slightly smaller decrease than under LD 12:12 and insulin-induced hypoglycemia led to a striking increase of NAT. As the changes in pineal NAT are brought about by rather strong exogenous stimuli it is suspected that the rat pineal gland during day-time is not very susceptible to ambient factors of normal range.
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PMID:The effects of a number of short-term exogenous stimuli on pineal serotonin-N-acetyltransferase activity in rats. 637 Nov 90

1. Insulin-induced hypoglycaemia is characterized by an autonomic disturbance which produces some of the symptoms of hypoglycaemia. How an additional autonomic stress like postural change may alter physiological responses and symptoms of hypoglycaemia is not known. In 10 healthy male subjects (mean age 24 years) we observed physiological and symptomatic responses to postural change during acute (20 min) and prolonged (60 min) hyperinsulinaemic (60 m-units min-1 m-2) hypoglycaemia (2.5 mmol/l) and euglycaemia (4.5 mmol/l), and placebo control (saline). 2. In all studies standing increased plasma catecholamines (adrenaline, P < 0.001; noradrenaline, P < 0.0001), blood pressure (P < 0.0001) and heart rate (P < 0.0001). Catecholamine responses to standing were augmented by acute hypoglycaemia (adrenaline, P < 0.005; noradrenaline, P < 0.01), but less so by prolonged hypoglycaemia (adrenaline, P < 0.05; noradrenaline, P < 0.05). Supine heart rate was higher before standing during prolonged hypoglycaemia (P < 0.05), but did not increase as much on standing when compared with acute hypoglycaemia and prolonged euglycaemia. 3. During acute hypoglycaemia, autonomic symptoms increased on standing, but during prolonged hypoglycaemia, in the presence of generally higher symptom scores, standing had no effect. Autonomic symptoms, with the exception of hunger, tended to decrease with time (P < 0.05) during prolonged hypoglycaemia. 4. To conclude, posture does modify the catecholamine and symptomatic responses to hypoglycaemia, but this effect is dependent on the duration of hypoglycaemia. Hypoglycaemia and hyperinsulinaemia had little or no effect on the cardiovascular responses to changing posture.
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PMID:Physiological and symptomatic responses to postural change in non-diabetic subjects during hypoglycaemia. 792 64

Suspected postprandial (reactive or idiopathic) hypoglycemia is characterized by predominantly adrenergic symptoms appearing after meals rich in carbohydrates and by their rare association with low blood glucose level (< 2.77 mmol/L). We studied heart rate, blood pressure, plasma insulin, C-peptide, and catecholamine responses during a 5-h oral glucose tolerance test in eight patients with suspected postprandial hypoglycemia and eight age-, sex-, and body mass index-matched healthy controls. We also evaluated beta-adrenergic sensitivity by using the isoproterenol sensitivity test. Psychological profile was assessed by the Symptom Checklist (SCL-90R) self-report symptom inventory. Patients with suspected postprandial hypoglycemia had higher beta-adrenergic sensitivity (defined as the dose of isoproterenol required to increase the resting heart rate by 25 beats/min) than controls (mean +/- SEM, 0.8 +/- 0.13 vs. 1.86 +/- 0.25 microgram isoproterenol; P = 0.002). After administration of glucose (75 g) blood glucose, plasma C-peptide, plasma epinephrine, and plasma norepinephrine responses were identical in the two groups, but plasma insulin was higher in the patients (group effect, P = 0.02; group by time interaction, P = 0.0001). Both heart rate and systolic blood pressure were significantly higher (but remained in the normal range) after glucose administration in patients with suspected postprandial hypoglycemia than in controls (group by time interactions, P = 0.004 and 0.0007, respectively). After glucose intake, seven patients had symptoms (palpitations, headache, tremor, generalized sweating, hunger, dizziness, sweating of the palms, flush, nausea, and fatigue), whereas in the control group, one subject reported flush and another palpitations, tremor, and hunger. Analysis of the SCL-90R questionnaire revealed that patients had emotional distress and significantly higher anxiety, somatization, depression, and obsessive-compulsive scores than controls. We may conclude that patients with suspected postprandial hypoglycemia have normal glucose tolerance, increased beta-adrenergic sensitivity, and emotional distress.
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PMID:Suspected postprandial hypoglycemia is associated with beta-adrenergic hypersensitivity and emotional distress. 796 39

A 67-year-old male was admitted with the complaint of weakness at hunger early in the morning, when blood glucose was less than 40 mg/dl. The abdominal ultrasonogram and computerized tomogram demonstrated a huge tumor in the right liver lobe. Hypoglycemia disappeared after transcatheter arterial embolization. Then hepatic lobectomy was performed. The tumor was histologically shown to be a fibrosarcoma. Insulin-like growth factor-II was intensely stained in the Golgi area of the tumor cells, suggesting its role in the mechanism of hypoglycemia.
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PMID:IGF-II producing hepatic fibrosarcoma associated with hypoglycemia. 820 62

1. To assess the influence of counterregulatory hormones, independently of neuroglycopaenia, on higher cerebral (cognitive) function, 'hypoglycaemic' warning symptoms and glucose kinetics, 10 healthy subjects participated in two hyperinsulinaemic (2 m-units min-1 kg-1) glucose clamp studies. After 100 min of euglycaemia (plasma glucose level 5 mmol/l), the plasma glucose level was either (a) maintained at 5 mmol/l for 120 min by glucose infusion with concomitant replacement of counterregulatory hormones (continuous infusions of glucagon, adrenaline, noradrenaline, cortisol and growth hormone) to mimic the hormonal milieu normally associated with hypoglycaemia (hormone infusion study) or (b) lowered to 2.8 mmol/l for 120 min (hypoglycaemia study). Assessments were made of cognitive function (P300 auditory evoked responses), symptoms (visual analogue scales) and glucose kinetics (3-[3H]glucose). 2. Hypoglycaemia was associated with an increase in all symptoms (facial flushing, palpitations, tingling, trembling, sweating, hunger, light-headedness and sleepiness, P < 0.01) and all subjects were aware that blood glucose levels had fallen. P300 evoked potential latency increased from 280 +/- 6 to 312 +/- 5 ms (mean +/- SEM, P < 0.01). In contrast, P300 latency and several individual symptoms (hunger, facial flushing, sweating and light-headedness) did not change from baseline during the hormone infusion study (P < 0.05 versus hypoglycaemia). Hepatic glucose production was lower (1.5 +/- 0.4 versus 2.3 +/- 0.3 mg min-1 kg-1, P < 0.05) and peripheral glucose uptake was higher (7.4 +/- 1.0 versus 5.6 +/- 0.6 mg min-1 kg-1, P < 0.01) during infusion of the hormones compared with during hypoglycaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of counterregulatory hormones, independently of hypoglycaemia, on cognitive function, warning symptoms and glucose kinetics. 840 88


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