Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bilateral 6-hydroxydopamine lesions of the nucleus accumbens septi (NAS) and olfactory tubercle (OT) caused enhanced intake of wet mash in 23-hr-food-deprived rats tested in photocell activity cages during restricted 30-min sessions. This mild hyperphagia was accompanied by a significant hypoactivity in the group with NAS/OT lesions. No hyperphagia was observed during a prolonged 120-min test session or in free-feeding tests conducted in the home cage. Anorexia induced by d-amphetamine (.5 and 1.5 mg/kg) was unaltered by the lesion, although the locomotor stimulant action of the drug was attenuated. A second experiment showed that the NAS/OT lesion also enhanced food intake in the photocell cages during 30-min sessions with dry food pellets but that food-associated drinking was concomitantly reduced. The results are consistent with the hypothesis that the behavioral changes caused by mesolimbic neuron destruction result in part from an inability to switch from one behavioral activity to another.
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PMID:Effects of 6-hydroxydopamine lesions of the nucleus accumbens septi and olfactory tubercle on feeding, locomotor activity, and amphetamine anorexia in the rat. 28 97

Surgical removal of the olfactory bulbs (OB) was performed in mature male red-winged blackbirds, maintained under a short-day light regime. Bulbectomy caused hyperphagia, which was not accompanied by obesity. Bulbectomized (OBX) birds had incresaed thyroid follicular activity and had greater developed testes than sham-operated controls. In the adenohypophyses of the OB-removed birds there was an increase in the populations of 4 types of chromophils: alcianophils, PAS-positive basophils, orangeophils and PAS-positive acidophils. The possibility that the OB are involved in the photoperiodic regulation of the activity of the gonads and thyroids is discussed.
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PMID:The involvement of the olfactory bulbs in the regulation of gonadal and thyroidal activities of male red-winged blackbirds, exposed to short-day light regime. 48 90

Surgical removal of the olfactory bulbs (O.B) in the chicken caused a marked increase in food intake, which was not accompanied by development of obestiy. Oxygen consumption of the O.B. removed birds was significantly higher than that of the controls. Alcianophylic-thyrotropic cell population of the adenohypophysis and the percentage of active follicles in the thyroid gland were higher for the O.B. removed birds than for those of the controls. Feed supplementation of 0.1% propylthiouracil to the O.B removed birds abolished the previously exhibited hyperphagia and caused a significant decline in oxygen consumption. The possibility that the O.B removal caused a primary increase in thyrotropic axis activity follwoed by a secondary compensatory hyperphagia, is discussed.
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PMID:Removal of olfactory bulbs in chickens: consequent changes in food intake and thyroid activity. 91 39

Neuropeptide Y (NPY) is a potent orexigenic agent capable of producing hyperphagia and obesity. NPY-containing neurons project from the hypothalmic arcuate nucleus to the paraventricular nucleus, an area known to be sensitive to the orexigenic effects of NPY. In this study we investigated the possibility that preproNPY messenger RNA (mRNA) content may be altered in obese Zucker rats compared to that of their lean littermates. Total RNA was isolated from hypothalamic dissections from male and female, obese and lean Zucker rats. RNA was also isolated from dissections of: olfactory bulb, entorhinal cortex, hippocampus, and striatum of female obese and lean rats. PreproNPY mRNA content was determined by solution hybridization-RNase protection analysis. The results revealed a 2- to 3-fold increase in preproNPY mRNA levels in the hypothalamus of obese animals compared to lean. The increase was observed in both sexes and was specific to the hypothalamus. In situ hybridization localized this increase to the arcuate nucleus. An additional RNase protection study was pursued to investigate the effects of 72 h food deprivation on hypothalamic preproNPY mRNA levels in lean and obese animals. Lean animals displayed an approximate 2-fold increase in preproNPY mRNA content, whereas obese animals showed no significant increase after food deprivation. These data are consistent with the hypothesis that NPY projections within the hypothalamus are involved in regulating feeding behavior and weight gain, and that disturbed regulation of hypothalamic NPY expression may play a role in the etiology of obesity in the genetically obese Zucker rat.
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PMID:Increased hypothalamic content of preproneuropeptide Y messenger ribonucleic acid in genetically obese Zucker rats and its regulation by food deprivation. 237 52

Bilateral basomedial hypothalamic (BMH) electrolytic lesions in White Leghorn cockerels produced six main physiological categories characterized by typical sets of symptoms: 1) functional castration (FC); hyperphagia, obesity, occasional diabetes insipidus, involuted adenohypophysis, dwarfism, atrophied comb and testes, reduced hematocrit, reduced plasma testosterone and thyroid activity, involuted thymus and adrenal cortex and elevated liver fat and plasma triglycerides and free fatty acids. The FC birds demonstrated defective immune response for the first 12 to 16 wk post-surgery. 2) functional castration with large comb (FCLC); hyperphagia, obesity, transient diabetes insipidus, slight diminution of adenohypophy-seal weight with marked reduction in basophilic cell population, fully atrophied testes but only slight reduction in comb size and hematocrit, plasma testosterone levels between those found in the first category and the control. 3) obese with normal testes (ONT); hyperphagia, obesity, high level of plasma lipids, normal histological organization of the adenohypophysis, normal testes, semen production and comb size. The next three categories exhibited physiological syndromes identical to the former three categories except for food intake, which operationally could be defined as normal. A marked difference among the BMH-lesioned birds was found in sexual behavior when the FC birds completely lost their libido. None of the replacement therapy regimens caused complete rehabilitation from adiposity or restoration of reproductive traits. Lipoprotein lipase activity increased at an early stage postlesioning and preceeded the development of hyperphagia. Placement of BMH lesions in newly hatched chicks resulted in marked dwarfism and obesity without hyperphagia. The BMH-lesioned heavy breed White Rock cockerels exhibited a lesser degree of adiposity than the light White Leghorn birds. Removal of the olfactory bulbs and destruction of the septal area resulted in increased thyroid activity, with secondary hyperphagia without obesity. In a short-term study, administration of sodium pentobarbital to the BMH area resulted in increased feeding. Conversely, glucose administration to the same area suppressed feeding in satiated but not in food-deprived chickens.
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PMID:Role of the basomedial hypothalamus in regulation of adiposity, food intake, and reproductive traits in the domestic fowl. 267 24

Insulin binding was measured in membrane particles prepared from the liver and several brain regions of 4-month-old female Zucker fa/fa (obese), Fa/fa (heterozygous), and Fa/Fa (lean) rats. High affinity insulin binding was decreased in the olfactory bulb of fatty (0.23 pmol bound/mg protein) and heterozygous (0.16 pmol/mg) rats compared with that in the lean controls (0.64 pmol/mg). Total binding was not changed in the cerebral cortex or hypothalamus. High affinity insulin binding was also decreased in the liver of both fatty (0.44 +/- 0.22 pmol/mg; P less than 0.01) and heterozygous (0.75 +/- 0.35 pmol/mg) animals compared with that in the lean rats (2.10 +/- 1.55 pmol/mg). This decreased binding is probably not due to down-regulation of receptors in the heterozygous rats, as they do not exhibit the hyperinsulinemia observed in the fatty rats. Rather, our findings suggest that there is a gene-related alteration in insulin binding in the Zucker rat, as low binding was observed in rats carrying either one (Fa/fa) or two (fa/fa) doses of the gene. We postulate that this central defect in insulin binding may contribute to inadequate perception of a central insulin feedback signal and to the hyperphagia observed in the obese rats.
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PMID:Brain and liver insulin binding is decreased in Zucker rats carrying the 'fa' gene. 389 61

The present study evaluated the efficacy of olfactory aversion conditioning in the management of overeating problems. 42 overweight female subjects were assigned to one of three treatment conditions: olfactory aversion therapy, attention placebo control, and no-contact control. One experimenter administered the 8-wk. treatment phase. The aversion therapy procedure entailed the pairing of selected target foods (CSs) with noxious odors (UCSs). There were 25 pairings of the CS and UCSs during each weekly session. Four noxious odors were employed, one each week, to prevent habituation to the UCS. The attention-placebo control procedure was identical except that "air" was substituted for the putative UCS of the aversion therapy condition. At the end of the treatment period the aversion therapy group had lost 4.7 lb.; the attention placebo controls had lost 3.6 lb. and the no-contact controls 0.5 lb. The difference between the aversion therapy group and the no-contact controls was significant and that between the attention placebo group and the no-contact controls approached significance. At a follow-up 8 wk. after the end of the treatment period the weights of all groups had risen to pretreatment levels and there were no differences between them. These results indicate that olfactory aversion therapy is not an efficient technique in promoting weight-loss.
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PMID:Olfactory aversion conditioning and overeating: a review and some data. 663 52

Olfactory bulbectomy was performed on wild male European hamsters at different phases of their circannual body weight rhythm. Olfactory bulbectomy was always followed by an immediate hyperphagia the magnitude of which varied with the time of the year it was performed. The bulbectomy did not affect the phase of the circannual body weight rhythm, although in certain cases the rhythm is attenuated or apparently phase-shifted. Hyperphagia was delayed by food restriction but reappeared when animals were placed on ad lib food. The possible role of olfactory bulbs in the regulation of body weight, and the possibility that the maintenance expenditure of the bulbectomized animals is higher than that of the controls are discussed.
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PMID:Hyperphagia and obesity after olfactory bulbectomy performed at different times of the year in the European hamster. 717 73

Lesions of the amygdala have long been known to produce hyperphagia and obesity in cats, dogs, and monkeys, but only recently have studies with rats determined that the effective site is the posterodorsal amygdala (PDA)-the posterodorsal medial amygdaloid nucleus and the intra-amygdaloid bed nucleus of the stria terminalis. There is a sex difference; female rats with PDA lesions display greater weight gain than male rats. In the brains of female rats with obesity-inducing PDA lesions, there is a dense pattern of axonal degeneration in the capsule of the ventromedial hypothalamus (VMH) and other targets of the stria terminalis. Transections of the dorsal component of the stria terminalis also result in hyperphagia and obesity in female rats. Similar to rats with VMH lesions, rats with PDA lesions are hyperinsulinemic during food restriction and greatly prefer high-carbohydrate diets. The PDA is also a critical site for some aspects of rodent sexual behavior, particularly those that depend on olfaction, and the pattern of degeneration observed after obesity-inducing PDA lesions is remarkably parallel to the circuit that has been proposed to mediate sexual behavior. Medial amygdaloid lesions disrupt the normal feeding pattern and result in impaired responses to caloric challenges, and there is evidence that these behavioral changes are also due to a disruption of olfactory input. With its input from the olfactory bulbs and connections to the VMH, the PDA may be a nodal point at which olfactory and neuroendocrine stimuli are integrated to affect feeding behavior.
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PMID:Amygdaloid lesion-induced obesity: relation to sexual behavior, olfaction, and the ventromedial hypothalamus. 1677 67

Complementary neurophysiological recordings in rhesus macaques (Macaca mulatta) and functional neuroimaging in human subjects show that the primary taste cortex in the rostral insula and adjoining frontal operculum provides separate and combined representations of the taste, temperature and texture (including viscosity and fat texture) of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex, these sensory inputs are for some neurons combined by learning with olfactory and visual inputs. Different neurons respond to different combinations, providing a rich representation of the sensory properties of food. In the orbitofrontal cortex feeding to satiety with one food decreases the responses of these neurons to that food, but not to other foods, showing that sensory-specific satiety is computed in the primate (including the human) orbitofrontal cortex. Consistently, activation of parts of the human orbitofrontal cortex correlates with subjective ratings of the pleasantness of the taste and smell of food. Cognitive factors, such as a word label presented with an odour, influence the pleasantness of the odour, and the activation produced by the odour in the orbitofrontal cortex. Food intake is thus controlled by building a multimodal representation of the sensory properties of food in the orbitofrontal cortex and gating this representation by satiety signals to produce a representation of the pleasantness or reward value of food that drives food intake. Factors that lead this system to become unbalanced and contribute to overeating and obesity are described.
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PMID:Sensory processing in the brain related to the control of food intake. 1734 76


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