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

Hungry rats display the characteristic "satiety sequence" after drinking a glucose solution: The end of ingestion is accompanied by grooming and exploring, followed by resting. With saccharin solutions over a range of concentrations, however, ingestion is accompanied and followed by persistent grooming and exploring; resting rarely occurs. Gastric preloads of glucose solution promote resting to reinstate the "satiety sequence" after a bout of saccharin ingestion. Therefore, the systemic effects of glucose are sufficient to promote resting. In the absence of postingestive factors, the "satiety sequence" is incomplete following saccharin ingestion as it is after sham-feeding.
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PMID:Behavioral correlates of oral and postingestive satiety in the rat. 652 91

In some isolated parts of North Africa, there persists an ancient Berber custom of imposing an overfeeding regimen on young girls before marriage, to achieve an obesity which is regarded as aesthetically pleasing. We have studied the effect of such a regimen, lasting 12--16 weeks, on blood lipids and on the affective reactions to sweet tastes in nine subjects. It is known that the pleasantness of alimentary cues i.e., the feeding behaviour, depends on the subject's nutritional state. Only three subjects gained weight (by 3,5 and 8 kg), in spite of the strong pressure to overeat. No change in plasma lipid concentrations were observed. Nevertheless, at the end of the regimen every subject showed a highly significant decrease in the rated pleasantness of sweet stimuli when they were tested fasting. However, the reduction in sweet pleasantness induced by ingestion of a 200 ml load of 1.4 M glucose solution was not changed by the overfeeding. Thus, pressure to overfeed can reduce hunger, as seen in the attractiveness of sweet foods in fasted subjects, without modifying glucose-induced satiety.
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PMID:Effects of an overfeeding regimen--the affective component of the sweet sensation. 658 99

Endogenous sugar acids, 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA) and 2,4,5-trihydroxypentanoic acid (3-deoxypentonic acid, 3-DPA), have been identified in the serum of fasted rats. Effects of these sugar acids on rat feeding behavior and neuron activity were investigated. Injections of 2-DTA (2.5 mumol) into the third cerebral ventricle of chronic rats suppressed food intake and single-neuron activity in the lateral hypothalamic area (LHA). Food consumption was reduced for 24 h, even in 72-h food-deprived rats. The same amounts of 3-DPA elicited feeding and increased LHA single-neuron activity with latencies of 6-8 min. Electrophoretically applied 2-DTA significantly and specifically suppressed activity of glucose-sensitive neurons in the LHA, whereas 3-DPA facilitated the activity. Nonglucose-sensitive LHA neurons were not affected by these sugar acids. The high correlation between modulation of feeding behavior and changes in LHA neuron activity after injection of these sugar acids suggested that 2-DTA may act as an endogenous satiety substance and 3-DPA as a hunger substance. The effects may be mediated through glucose-sensitive neurons in the LHA.
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PMID:Modulation of feeding by endogenous sugar acids acting as hunger or satiety factors. 672 Sep 28

As a weight-losing adjunct, 7.5 g glycerol in a 25 per cent solution was administered before meals to members of a commercial weight-reducing club. The same amount of glucose served as placebo. Members were randomly given either solution for six weeks. Body weight and hunger ratings were recorded weekly. Thirty-one members completed the study. Initial mean body weight was 77.5 +/- 12.9 (s.d.) kg corresponding to a Broca index of 1.16 +/- 0.18. Members on glycerol lost 4.1 +/- 2.2 kg and those on glucose lost 3.2 +/- 2.4 kg (n.s.). At the onset of the meal, plasma glycerol concentration was about ten times above baseline values. The study extends previous observations made in smaller groups that glycerol does not improve weight loss in subjects on a hypocaloric diet.
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PMID:Effects of glycerol addition to diet in weight-reducing clubs. 672 94

Feeding-related neuronal activity of lateral hypothalamic glucose-sensitive and glucose-insensitive neurons was investigated in behaving monkeys. The behavioral paradigm was a high fixed ratio of bar pressing for food reward signaled by light and tone cues. Twenty-seven percent of the neurons tested were glucose-sensitive. The population of neurons which changed in firing rate during the feeding task was higher among glucose-sensitive cells than among glucose-insensitive cells. The activity of many glucose-sensitive neurons decreased during the bar pressing and reward periods. A small population of glucose-sensitive neurons responded to cue stimuli. The results suggest that glucose-sensitive neurons are mainly involved in the drive and/or reward mechanism of feeding behavior, and that these cells may have specific roles in neural control of hunger-motivated food acquisition.
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PMID:Behavioral significance of monkey hypothalamic glucose-sensitive neurons. 673 7

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

It has been suggested for a long time that the metabolic stimulation to eat or the hunger arousal of eating, originated from a fall in the blood glucose level induced by the periodic failure of hepatic glucose production to match the peripheral glucose uptake. However, this suggestion has not been substantiated directly by the results of periodic blood glucose evaluations performed during intermeal intervals in free-fed rats. In this experiment, a technique involving a continuous blood glucose determination over several hours was used in free-feeding, undisturbed rats. It was shown that all nocturnal and diurnal meals were preceded by a 6 to 8% fall of blood level, starting 5 to 6 min prior to meal onset. The overall consequences of these findings are discussed.
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PMID:Fall in blood glucose level precedes meal onset in free-feeding rats. 676 4

Detailed endocrine studies were carried out in 95 hospitalized obese patients during their treatment with diet and the tricyclic anoretic mazindol. The results obtained after 1 week or more of mazindol (2 mg or occasionally 4 mg/day) administration were compared with the results after placebo and with the initial pre-treatment values. There were no significant changes in the following parameters: FSH, LH, testosterone, renin, angiotensin II, growth hormone (GH) levels during insulin tolerance tests (ITT), 131I uptake, basal metabolic rate, Achilles tendon reflexes, T3 RIA, rT3 RIA, 17-ketosteroids and 17-ketogenic steroids in urine, both basal and after stimulation with ACTH and metyrapone. Blood glucose and plasma immunoreactive insulin (IRI) levels during oral glucose tolerance tests decreased during mazindol administration, IRI levels were significantly lower during ITTs after mazindol. T4 RIA serum levels increased significantly after mazindol. When mazindol was administered, GH levels increased somewhat in some obese patients during ITTs, while T3 RIA and rT3 RIA decreased in some patients. Mazindol has not only hunger (appetite) suppressing properties, but it probably affects the metabolism of energy substrates as well. The drug was well tolerated and there were no pathological findings in routine laboratory examinations during a long-term study with mazindol (non-stop treatment for 6 months).
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PMID:Endocrine studies with mazindol in obese patients. 677 43

Hungry rats were permitted to drink a concentrated glucose solution to 'satiety', as indicated by (1) cessation of drinking, (2) the appearance of behaviors correlated with satiety (grooming and exploring followed by resting), and (3) refusal to drink appreciable further quantities when access to the solution was prolonged. Yet such rats returned to vigorous and prolonged feeding when offered laboratory pellets, powered chow, or even glucose itself in powered form. "Satiety" for a glucose solution does not reflect a generalized suppression of hunger or of a specific carbohydrate hunger. Its properties are more specific than existing theories of energy intake regulation would lead us to suppose.
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PMID:Glucose solution intake in the rat: the specificity of postingestive satiety. 688 57

Physiological changes accompanying a period of voluntary hypophagia in male Sprague-Dawley rats after insulin-induced hyperphagia and body weight gain were investigated. Postinsulin hypophagia was manifested as a reduction in meal duration diurnally and nocturnally (Geary et al., Behav. Neural Biol. 31: 435-442, 1981). Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats, suggesting a postabsorptive mechanism controlled the hypophagia. Basal blood glucose and plasma nonesterified fatty acids, 3-hydroxybutyrate, glycerol, and some amino acids were elevated during hypophagia, while liver glycogen content was reduced. Hypophagic rats' arteriovenous blood glucose differences and glucose oxidation rates, however, were not different from controls. After nutrient repletion blood glucose and plasma glycerol remained elevated in hypophagic rats in comparison to controls, while differences in other plasma metabolites were reduced. Liver glycogen accumulated faster in hypophagic rats. These data were related to the lipostatic and other hypotheses how energy balance status affects hunger and satiety.
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PMID:Blood metabolites and feeding during postinsulin hypophagia. 705 64


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