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

A squirrel monkey, if it needs a particular dietary component because of a metabolic disorder or because that food has been excluded from its diet, will develop a specific hunger for the food. In cases where specific hungers show up clearly, four behaviors can be demonstrated: (1) The monkey prefers the food it needs to other foods that are also available; (2) It usually ingests large amounts of the food to meet its particular physiological requirements; (3) The animal will tend to eat the needed food even while the stomach is full; (4) When vitamin B2 is removed from its diet, a squirrel monkey will exhibit digestive disturbance, general weakness, a lack of vigor, and loss of weight.
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PMID:Experimental studies of food selective behavior in squirrel monkeys fed on riboflavin deficient diet. 81 66

The allocation of some symptoms of acute hypoglycaemia to autonomic and neuroglycopenic groups has proved problematical, with possible misinterpretation of studies which depend upon the use of diverse symptom questionnaires. Two hundred and ninety-five randomly selected insulin-treated diabetic patients were asked to report the symptoms which they usually experienced and believed to be caused by hypoglycaemia. Sweating, trembling, inability to concentrate, weakness, hunger and blurred vision were the most frequently reported symptoms. To classify symptoms of hypoglycaemia objectively, Factor Analysis was used to identify related symptoms which grouped together. This resulted in five groups or clusters of symptoms, four of which could be denominated as groups with a presumed common aetiology, and were labelled: 'neuroglycopenic', 'general malaise', 'autonomic', 'motor dysfunction', and 'sensory dysfunction'. The groups of symptoms derived by Factor Analysis were assessed in relation to partial or absent symptomatic awareness of hypoglycaemia based on historical evidence from the 295 insulin-treated diabetic patients. Neuroglycopenic symptoms were reported more commonly by the patients who had reported partial awareness of hypoglycaemia (number of symptoms 2.6 +/- 1.8 (mean +/- SD] than by the patients who had reported normal hypoglycaemia awareness (1.4 +/- 1.5 symptoms) (p less than 0.05). By contrast autonomic symptoms were reported less frequently by the patients who had reported absent hypoglycaemia awareness (1.3 +/- 1.4 symptoms) than by those with normal awareness (2.2 +/- 1.4 symptoms) (p less than 0.05), which was similar to the number of autonomic symptoms reported by the patients who had partial hypoglycaemia awareness (2.1 +/- 1.3 symptoms).
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PMID:Classification of symptoms of hypoglycaemia in insulin-treated diabetic patients using factor analysis: relationship to hypoglycaemia unawareness. 155 13

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

Two experiments were designed to investigate the neurobehavioral effects of phenylalanine (PHE; 0.84, 2.52, 5.04, and 10.08 g) and aspartame (APM; 5.04 and 10.08 g) on energy and macronutrient selection and on subjective feelings of hunger, mood and arousal in normal weight adult males. Neither phenylalanine nor aspartame altered mean energy intakes or macronutrient selection at a lunch begun 60 to 105 min after the amino acids were consumed. During this time, increased (p less than 0.05) visual analog scale (VAS) scores for emptiness, rumbling, weakness, degree of hunger and urge to eat were found in both experiments, but no treatment effects or interactions were seen for any variable in either experiment. Plasma PHE levels and ratios to other large neutral amino acids (NAA) rose significantly (p less than 0.05) after all treatments except 0.84 g PHE; plasma tyrosine (TYR) levels increased (p less than 0.05) only when greater than or equal to 2.52 g PHE was given. TYR/NAA ratios were higher (p less than 0.05) after 2.52 and 5.04 g PHE, and 10.08 g APM. No relationships were found between food intake and plasma amino acid levels. We conclude that, in normal weight men, PHE and APM, in doses up to 10 g, do not affect short-term energy and macronutrient intakes, or subjective feelings of hunger, mood and arousal.
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PMID:Phenylalanine and aspartame fail to alter feeding behavior, mood and arousal in men. 793 34

In a summer camp for 47 diabetic children in Kinki district, Japan, in 1984, the relationship between hypoglycemic symptoms and blood glucose levels by self-monitoring was analyzed. During the 7-day camp, self-monitoring of blood glucose (SMBG) was carried out 599 times in total, 12.7 times per camper. SMBG due to hypoglycemic complaints amounted to 371. 154 measurements out of 371 indicated blood glucose levels under 80 mg/dl, but 78 monitorings were found to be over 200 mg/dl. Fatigue or weakness were the most frequent hypoglycemic symptoms, as was hunger sensation, each reaching approximately 40% in frequency. In most complaints of tremor, the blood glucose level was critically low. Prompt measurement of blood glucose is indeed necessary to properly treat diabetic children with 'hypoglycemic' symptoms.
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PMID:Relationship between hypoglycemic symptoms and blood glucose levels due to self-monitoring in summer camp for diabetic children in Japan. 383 7

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

With the conventional method of fasting or aggressive dieting to reduce excess body fat, hunger, weakness, ketogenesis and ketosis are the sequential events that follow. It is not fully understood why, under conditions of negative calorie balance where complete energy release from storage fat is critical, ketosis should arise with a concomitant wastage of energy. Here, I wish to propose a theory that relates the formation of ketone bodies under such conditions to a deficiency in dietary pantothenic acid. Supplementation of this vitamin would facilitate complete catabolism of fatty acids and thus the formation of ketone bodies could be circumvented. As a result, a sufficient amount of energy would be released from storage fat to relieve dieters of the sensation of hunger and weakness which otherwise would be difficult to endure. Hence, using this method for weight reduction together with a careful observation of calorie intake, I have great success in treating overweight-to-obese patients to lose weight.
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PMID:Pantothenic acid as a weight-reducing agent: fasting without hunger, weakness and ketosis. 858 72

There is an asymmetry in the operation of physiological processes that maintain body weight. The body exerts a strong defence against undernutrition and weight loss, but applies a much weaker resistance to overconsumption and weight gain. These principles influence how appetite control operates and this constitutes one form of vulnerability to weight gain. The expression of appetite is reflected in an episodic pattern of eating behaviour, the selection of dietary commodities and an associated profile of conscious sensations such as hunger, preferences, aversions and fullness. The onset and termination of eating episodes are subject to facilitatory and inhibitory physiological processes, and are held in place by strong environmental contingencies and habitual routines. Energy intake resulting from physiological and environmental control of behaviour is generally in balance with energy expenditure, although changes in energy expenditure do not inevitably trigger changes in food intake. Excess energy intake over expenditure may be due to aberrant positive drive to seek energy or a permissive response to strong external stimuli. The former could arise from a defect in a lipostatic regulatory system, and the latter from the weakness of inhibitory signals or from strong facilitatory responses to superpotent physical features of food. Taste and textural qualities of food give rise to hedonic responses via opioidergic and aminergic systems. Inhibitory responses to macronutrients include adjustment of gastric volume, rate of gastric emptying, release of cholecystokinin and enterostatin, and changes in plasma levels of products of digestion. These peripheral responses lead to a series of changes in brain neurotransmitter networks. Proteins, fats and carbohydrates generate different sets of physiological responses that produce different effects on the intensity and duration of satiety. The nutrient composition of food and the overall energy density influence control of meal size and post-ingestive inhibition. Particular sensory and nutrient combinations in foods can facilitate passive overconsumption. Overriding physiological satiety signals can lead to a positive energy balance and weight gain.
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PMID:Overconsumption as a cause of weight gain: behavioural-physiological interactions in the control of food intake (appetite). 901 79

Symptomatic episodes of documented hypoglycaemia were characterized with the aid of a 3-month diary in a single-centre, unselected group of 161 children and adolescents with Type 1 diabetes mellitus, treated mainly (81%) with multiple-dose insulin therapy. Patients and families were asked to write in the diary all the symptomatic episodes in which blood glucose concentration proved to be < or =3 mmol l(-1) before treatment. Of the patients, 83 (52%) had a total of 287 hypoglycaemic episodes (0.6 attack per month per patient). The majority of the attacks, 221 (77%), were mild (patients > or =6 years able to treat themselves). Only two attacks were severe, resulting in coma and/or convulsion. The most common dominant symptoms were weakness (29%), tremor (20%), hunger (14%), and drowsiness (12%). Of all the dominant symptoms, 39% were classified as autonomic, 20% neuroglycopenic, and 41% non-specific. In children under 6 years, autonomic symptoms were less common than in adolescents 15 years or over (34% vs 57%, p = 0.01). In conclusion, the incidence of documented symptomatic hypoglycaemia was low. The symptoms were more often neuroglycopenic or non-specific than autonomic, especially in young children.
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PMID:Documented symptomatic hypoglycaemia in children and adolescents using multiple daily insulin injection therapy. 963 24

We report a case of hypoglycaemic shock which occurred in a patient 18 h after injury. The patient was involved in a road traffic accident and sustained multiple rib fractures and bruising in the (R) lumbar region. Eleven hours after his last meal he developed sudden weakness, profuse sweating, air hunger, thirst, disorientation and suddenly lapsed into coma 18 h after admission. Administration of 50 ml of 50% dextrose resulted in immediate restoration of consciousness. This case shows that this complication can occur in trauma patients even though the metabolic response to trauma is usually assumed to be hyperglycaemic.
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PMID:Hypoglycaemic shock: normal or abnormal response to injury? 1041 12


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