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

Although subjective appetite scores are widely used, studies on the reproducibility of this method are scarce. In the present study nine healthy, normal weight, young men recorded their subjective appetite sensations before and during 5 h after two different test meals A and B. The subjects tested each meal twice and in randomized order. Visual analogue scale (VAS) scores, 10 cm in length, were used to assess hunger, satiety, fullness, prospective food consumption and palatability of the meals. Plasma glucose and lactate concentrations were determined concomitantly. The repeatability was investigated for fasting values, delta-mean 5 h and mean 5 h values, delta-peak/nadir and peak/nadir values. Although the profiles of the postprandial responses were similar, the coefficients of repeatability (CR = 2SD) on the mean differences were large, ranging from 2.86 to 5.24 cm for fasting scores, 1.36 to 1.88 cm for mean scores, 2.98 to 5.42 cm for delta-mean scores, and 3.16 to 6.44 cm for peak and delta-peak scores. For palatability ratings the CR values varied more, ranging from 2.38 (taste) to 8.70 cm (aftertaste). Part of the difference in satiety ratings could be explained by the differences in palatability ratings. However, the low reproducibility may also be caused by a conditioned satiation or hunger due to the subjects' prior experience of the meals and therefore not just be a reflection of random noise. It is likely, however, that the variation in appetite ratings is due both to methodological day-to-day variation and to biological day-to-day variation in subjective appetite sensations.
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PMID:The reproducibility of subjective appetite scores. 779 69

The authors studied the behavior of body weight, blood glucose, total serum cholesterol, and hunger and satiety sensation in 30 patients treated for 60 days with a 1.200 kcal (5040 kj) diet plus either placebo or glucomannane. All the variables considered show that the low-calorie diet plus glucomannane is more effective than the low-calorie diet alone.
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PMID:[Evaluation of the action of glucomannan on metabolic parameters and on the sensation of satiation in overweight and obese patients]. 779 58

Anorexia nervosa (AN) is associated with a paradoxical reduction in hunger ratings following 2-deoxy-D-glucose (2DG) induced glucose insufficiency. Because of the relationship between exercise and AN, there is interest in the weight-loss phenomenon produced by exercise in food restricted rats. This investigation determined if the weight-loss phenomenon is associated with a paradoxical suppression of food intake following 2DG and if the effect is related to reductions in prevailing glucose and insulin levels. Weight-matched, normal-weight exercised and normal-weight unexercised rats served as controls. As predicted, 2DG reduced food intake in animals subjected to the phenomenon (1.5 h/day food access and 22.5 h/day running wheel access). This effect was related to reductions in plasma glucose and insulin under the conditions that prevailed at the time of injection. Since these changes also occurred in weight-matched controls, they were attributed to the general effects of weight loss. A situational specificity for the "anorexia" of the weight-loss syndrome was also demonstrated. Finally, the strengths and weaknesses of the phenomenon as a model of AN were considered.
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PMID:Exercise in food-restricted rats produces 2DG feeding and metabolic abnormalities similar to anorexia nervosa. 787 8

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

There is considerable evidence that hepatic vagal afferents monitor the availability of liver glycogen and glucose metabolites, and that this mechanism participates in appetite regulation. Thus, promotion of gluconeogenesis and liver glycogen storage may enhance satiety. Hepatic lipid oxidation drives gluconeogenesis by positive allosteric modulation of pyruvate carboxylase and fructodiphosphatase. The rate-limiting enzyme for hepatic lipid oxidation, carnitine acyltransferase I, is activated by exogenous carnitine, and inhibited by malonyl coA. The lipogenesis inhibitor (-)-hydroxycitrate--a natural fruit acid found in the Brindall berry--can decrease production of malonyl coA in hepatocytes by potent inhibition of citrate lyase; many studies demonstrate that (-)-hydroxycitrate can reduce body fat accumulation in growing rats, owing in large part to a reduction in appetite. Joint administration of (-)-hydroxycitrate and carnitine should therefore promote hepatic lipid oxidation, gluconeogenesis, and satiety. Thermogenic effects as well as a reduction of the respiratory quotient can also be predicted. If this technique proves clinically useful in weight management, it could be used in conjunction with chromium picolinate and soluble fiber supplements, which appear to aid hunger control at the level of the hypothalamus and terminal ileum, respectively.
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PMID:Promotion of hepatic lipid oxidation and gluconeogenesis as a strategy for appetite control. 807 27

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

Experiments indicate that exposure to high-carbohydrate foods can give rise to a clear modulation of the expression of human appetite. The potency and time course of the effects of various carbohydrates on satiety vary with the amount consumed and the chemical structure. There is evidence that this biological effect can modulate the temporal profile of hunger and the eating pattern of meals and snacks. One important issue is the action of carbohydrate foods on satiation (within meals) and satiety (after meals). These effects can be compared with the effects of high-fat foods. The physiological mechanisms through which carbohydrates exert an action on appetite are not completely identified, although plasma glucose values are likely to play a role. The experimental evidence suggests that it is possible to design high-carbohydrate diets that provide good nutrition with adequate control over appetite and a beneficial effect on body weight.
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PMID:Carbohydrates and human appetite. 811 57

Strenuous training in women has been shown to cause menstrual dysfunction and decreased bone mineral density. These endocrine and metabolic complications are associated with an insufficient dietary intake and decreased body fat content in female athletes. The present investigation was undertaken to study serum levels of cholecystokinin (CCK), insulin, gastrin, and cortisol in 14 female long-distance runners and 15 sex- and age-matched control subjects during intake of a standardized meal (500 kcal). The athletes showed a decreased response of the "satiety peptide" CCK to the meal and reported increased hunger compared with the control group. Meal-related insulin response was also decreased in the athletes, whereas gastrin levels were comparable to those of controls. Basal levels of glucose were increased in the athletes, but there was no difference in postprandial levels between the groups. Cortisol levels were clearly elevated in the female runners. We conclude that insufficient food intake in female athletes cannot be explained by increased CCK secretion and satiety. Since the athletes reported a larger caloric intake of a normal daily breakfast than the control subjects, the decreased CCK response may instead be explained by an adaptation to increased food intake. The decreased meal-related insulin response may be a reflection of increased insulin sensitivity as an adaptation to physical exercise. However, an impaired peptide secretion cannot be excluded. The role of elevated cortisol levels in the gastrointestinal hormone response needs further investigation.
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PMID:Reduced serum cholecystokinin response to food intake in female athletes. 812 5

A review of published data shows that although intense sweeteners have been shown to increase hunger ratings in some studies in humans, this has not been a consistent and reproducible observation. Any slight effect on perceived hunger has not been translated into an increase in food ingestion or effects on blood concentrations of insulin or glucose. Studies on the covert substitution of caloric sweeteners by intense sweeteners have shown either a decrease or no change in body weight. The published database does not support the concept that the consumption of intense sweeteners results in a paradoxical increase in calorie intake and body weight.
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PMID:Intense sweeteners, food intake, and the weight of a body of evidence. 814 Jan 58

The objective of this study was to compare glycemic thresholds for hypoglycemic responses in obese and control subjects. A modified glucose-clamp technique was used to produce a standardized fall in plasma glucose (0.5 mmol/l per 40 min) in nine morbidly obese and ten control subjects. The release of the counter-regulatory hormones was measured and a symptom questionnaire was filled out every 10 min. The hypoglycemic thresholds (taken as the plasma glucose level where the response exceeded the basal level +2 s.d.) were practically identical in the two groups both for the hormones and the symptoms (including hunger). Our results argue against the hypothesis that an increased sensitivity to a falling plasma glucose is of importance in the pathogenesis of obesity.
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PMID:Glycemic thresholds for hypoglycemic responses in obese subjects. 814 24


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