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

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

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.
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PMID:Endocrine emergencies. Hypoglycaemia. 173 95

Hexoses infused slowly into the duodenum or hepatic-portal vein reduce feeding. However, hexoses can increase food intake following rapid infusion via either of these two routes. Insulin responses and resultant glycemic changes differ following fast and slow duodenal glucose infusion. This is unlikely to be the primary explanation, because fructose affects feeding but is not a secretagogue of insulin under our testing conditions. In follow-up studies, we infused glucose or fructose into the hepatic-portal vein at the fast or the slow rate, and measured 14C incorporation into liver mitochondria and glycogen, and tritiated water uptake into hepatic lipids. Fast infusion of glucose or fructose increased lipid formation, reducing mitochondrial uptake and glycogen formation, and was associated with hunger enhancement. Slow hexose infusion was associated with substrate uptake into mitochondria and glycogen, with reduced uptake into hepatic fat. These findings all are consistent with the previously observed positive correlation seen between mitochondrial oxidation and satiety (28).
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PMID:The metabolic bases for "paradoxical" and normal feeding. 195 42

Fifteen normal volunteers received one insulin injection or saline in two nonconsecutive days. At 0', 30', 60' and 90' water intake was measured. Simultaneously subjective thirst and hunger were recorded by running a set of psychological tests. Water intake was higher after insulin than saline at 60' and 90'. Insulin increases thirst sensation even before the sensation of hunger.
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PMID:Psychological aspects of insulin-induced thirst. 201 69

Rats injected subcutaneously with 5 U/kg of regular insulin increased food intake above control levels in a 2 hr test and showed a median latency to eat of 59 min. One week later, rats were injected again with saline or insulin (5 U/kg), deprived of food and killed 60 +/- 10 min later. Insulin treatment produced a marked reduction in plasma glucose, plasma ketone bodies and liver glycogen, as well as a marked acceleration of gastric emptying. The results indicate that a variety of changes in peripheral metabolism and physiology may underlie the increase in food intake observed after insulin injection and that it is premature to ascribe the hunger-inducing effect of insulin treatment solely to a decline in blood glucose.
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PMID:Metabolic and physiologic effects of a hunger-inducing injection of insulin. 675 87

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

Diabetes mellitus is a metabolic disorder which has affected several millions of population all over the world. It is characterized by an excess of sugar in the blood and urine, hunger, thirst and gradual loss of weight. Insulin is a hormone which regulates the carbohydrate and triacylglyceride metabolism through its action at several sites and facilitates the entry of glucose accumulation in the blood. Insulin also stimulates the synthesis of glucokinase and moderates the degree of gluconeogenesis. In the diabetic patient, there is an aberration in the functioning of insulin. Prior to the 1950s, control of diabetes was based entirely on insulin therapy. Unfortunately, some patients developed complications and thus need for some other therapy was realized. Presently control of NIDDM relies on compounds from two classes--sulphonylureas and biguanides. Although these drugs are widely accepted as being efficacious in treating some diabetics, they are ineffective in many others. Consequently, testing of many chemicals and plant extracts has continued. The object of the present paper is to bring up-to-date information on the hypoglycemic activity of plants, above all the plants occurring in our country, and those who se hypoglycemic activity has been scientifically documented in a more detailed way. Recent theories on the mechanism of action of these plants are also discussed.
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PMID:[Plants with hypoglycemic effects]. 811 60

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

A 59-year-old female with 20-year history of slowly progressing muscle atrophy and sensory disturbance of upper extremities showed short stature, scoliosis, hunger type of sensory dissociation of the upper extremities and pyramidal tract sign of the lower extremities. Magnetic resonance imaging (MRI) clarified hypoplasia of the anterior pituitary lobe, Arnold-Chiari malformation and cervical syringomyelia. Insulin and arginine stimulating tests revealed partial type of isolated growth hormone (GH) deficiency but GH gene analysis detected no defects of GH genes. It was considered to be a rare case of non-hereditary hypopituitarism with Chiari malformation and syringomyelia not associated with perinatal injury, namely a midline anomaly syndrome.
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PMID:Isolated partial growth hormone deficient short stature with syringomyelia not associated with birth injury. 974 53

Adipose tissue performs complex metabolic and endocrine functions. Among the endocrine products produced by adipose tissue are tumour necrosis factor alpha, interleukin 6, acylation-stimulating protein and leptin. The present review will focus primarily on mechanisms regulating leptin production and leptin action, and the implications of this regulation in the control of energy balance. Leptin acts in the central nervous system where it interacts with a number of hypothalamic neuropeptide systems to regulate feeding behaviour and energy expenditure. The presence of extreme obesity in animals and human subjects with mutations of the leptin gene or the leptin receptor demonstrates that normal leptin production and action are critical for maintaining energy balance. Insulin is the major regulator of leptin production by adipose tissue. Insulin infusions increase circulating leptin concentrations in human subjects. Plasma leptin levels are markedly decreased in insulin-deficient diabetic rodents, and the low leptin levels contribute to diabetic hyperphagia. Based on in vitro studies, the effect of insulin to stimulate leptin production appears to involve increased glucose metabolism. Blockade of glucose transport or glycolysis inhibits leptin expression and secretion in isolated adipocytes. Evidence suggests that anaerobic metabolism of glucose to lactate does not stimulate leptin production. Alterations in insulin-mediated glucose metabolism in adipose tissue are likely to mediate the effects of energy restriction to decrease, and refeeding to increase, circulating leptin levels. Changes in glucose metabolism may also explain the observation that high-fat meals lower 24h circulating leptin levels relative to high-carbohydrate meals in human subjects, suggesting a mechanism that may contribute to the effects that high-fat diets have in promoting increased energy intake, weight gain and obesity. The decreased circulating leptin observed during energy restriction is related to increased sensations of hunger in human subjects. Thus, decreases in leptin during energy-restricted weight-loss regimens may contribute to the strong propensity for weight regain. A better understanding of the precise mechanisms regulating leptin production and leptin action may lead to new approaches for managing obesity.
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PMID:Role of adipose tissue in body-weight regulation: mechanisms regulating leptin production and energy balance. 1099 52


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