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)

Electroosmotic applications of 2-deoxy-D-glucose (2-DG) were made in the lateral hypothalamus (LHA). Changes in LHA unit activity and concomitant gastric acid secretion were then observed 2-DG responsive neurons tended to form two clusters in the LHA. Electroosmotic application induced four patterns of activity change in different LHA neurons. Gastric acid secretion increased when LHA unit activity increased. Results presented here agree with prior reports of hypophagia after precise lesions in this LHA region and other reports of 2-DG induced hyperphagia which might be mediated through central neurons.
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PMID:Lateral hypothalamus neuron responses to electroosmotic 2-deoxy-D-glucose. 713 57

To investigate the possible role of the area postrema (AP) in the control of food intake and body weight, male albino rats were divided into four groups: (a) animals dieted to 80% of their original body weights prior to receiving AP lesions, (b) nondieted animals with AP lesions, (c) animals dieted to 80% prior to receiving sham lesions, and (d) nondieted animals with sham lesions. Lesions of the AP in nondieted rats resulted in hypophagia, hypodipsia and body weight loss followed by recovery of normal intake and maintenance of body weight at a fixed percentage of the sham operated animals' weight. Reducing body weight prior to surgery led to body weight maintenance levels equivalent to those of the nondieted groups. We also tested the animals for sensitivity to glucoprivation caused by intraperitoneal injections of 2-deoxy-D-glucose (2-DG). Injections of 2-DG produced hyperphagia in sham lesioned rats, but not in rats with AP lesions. Our data suggest that the effects of AP lesions on intake and body weight are similar, in several important respects, to the lateral hypothalamic feeding syndrome and to the effects of subdiaphragmatic vagotomy. We discuss the results with respect to hierarchical levels of neural circuitry involved in controlling feeding behavior.
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PMID:Area postrema lesions produce feeding deficits in the rat: effects of preoperative dieting and 2-deoxy-D-glucose. 715 25

The glucose analogue, 2-deoxy-D-glucose (2-DG) elicits hyperphagic and analgesic responses in rats. The former response appears to be mediated by central processes since overeating is elicited following intraventricular administration of 2-DG at low (3.5 and 5.0 mg/kg) doses. The present study examined whether flinch-jump threshold would increase 30, 90 and 180 min following intraventricular injections of 2-DG at low (3.5, 5.0 and 10.0 mg/kg) doses and compared these effects with systemically-applied 2-DG doses of 350 and 500 mg/kg. Intraventricular 2-DG administration increased jump thresholds for up to 180 min across all test doses. Flinch thresholds were also increased, but in a manner dissociated from jump thresholds. Animals with cannulae located near, but not in the lateral ventricle, displayed delayed analgesic effects. The magnitude of intraventricular 2-DG analgesia was not at potent as the 100-fold higher systemic injections. It appears that central mechanisms mediated intraventricular 2-DG analgesia at the low dose range since higher, systemic 2-DG doses have previously failed to increase flinch-jump thresholds.
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PMID:Analgesia following intraventricular administration of 2-deoxy-D-glucose. 723 79

In male Sprague Dawley rats, the (-)-isomer of the opiate antagonist GPA 1843 (beta-9-methyl-5-phenyl-2-allyl-2'-hydroxy-6, 7-benzomorphan) produced dose-related decreases in nocturnal feeding and of hyperphagias induced by 2-deoxy-D-glucose (2-DG; 400 mg/kg) and 24 hr food deprivation (FD). The hyperphagia induced by insulin (10 U/kg) was not significantly decreased by GPA 1843. In contrast, comparable doses of the (+)-stereoisomer, GPA 1847, had no effect on nocturnal, 2-DG or FD hyperphagia. In addition, hyperphagia and hyperdipsia were observed following administration of the opiate agonist levorphanol, but not its stereoisomer, dextrorphan. Thus, the effects of these agents on consummatory behavior are mediated by a stereospecific interaction with opiate receptors, which further indicates that endogenous opiate peptides are involved in the expression of these opiate-related hyperphagias.
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PMID:Stereoselective effects of opiate agonists and antagonists on ingestive behavior in rats. 729 Dec 63

Drugs, such as sodium mercaptoacetate and methylpalmoxirate, which block fatty acid oxidation at different levels in the metabolic pathway, stimulate feeding. It is well known that selective centrally induced stimulation of dopamine, serotonin (5-hydroxytryptamine, 5-HT) and beta-adrenoceptors, or inhibition of the opiatergic system substantially decrease food intake in rats trained to eat 4 h a day. The results of the present study show that centrally acting dopaminergic and serotoninergic anorectic drugs, the opiate receptor antagonist naloxone, the alpha-adrenoceptor blocking drug phentolamine, and peripherally administered 5-HT counteract the overeating induced by mercaptoacetate. Comparing these effects to those described in 2-deoxy-D-glucose- and insulin-induced feeding, our data support the proposition that distinct neural circuits are involved in the hyperphagic responses to diverse metabolic stimuli.
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PMID:Pharmacological antagonism of lipoprivic feeding induced by sodium mercaptoacetate. 760 Dec 16

While opioid agonists administered into the hypothalamic paraventricular nucleus increase food intake in rats, naloxone reduces deprivation-induced intake. Ventricular administration of either mu (beta-funaltrexamine) or kappa (nor-binaltorphamine) opioid antagonists reduces spontaneous, deprivation, glucoprivic and palatable intake. The present study assessed whether microinjections of either general, mu or kappa opioid antagonists into the paraventricular nucleus altered either deprivation (24 h) intake, 2-deoxy-D-glucose hyperphagia or sucrose intake in rats. Deprivation intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 30-33%), beta-funaltrexamine (5 micrograms, 100 nmol, 26-29%) or naltrexone (10 micrograms, 260 nmol, 26%) in the paraventricular nucleus. 2-Deoxy-D-glucose hyperphagia was significantly reduced only after 2 h by naltrexone (10 micrograms, 260 nmol, 69%), norbinaltorphamine (20 micrograms, 272 nmol, 69%) or beta-funaltrexamine (20 micrograms, 400 nmol, 83%) in the paraventricular nucleus. Sucrose intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 27-36%), naltrexone (5-10 micrograms, 130-260 nmol, 18-31%) and beta-funaltrexamine (5 micrograms, 100 nmol, 20%) in the paraventricular nucleus. These data indicate that general, mu and kappa opioid antagonists administered into the hypothalamic paraventricular nucleus produce similar patterns of effects upon different forms of food intake as did ventricular administration, implicating this nucleus as part of the circuitry underlying opioid mediation of ingestion.
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PMID:Alterations in deprivation, glucoprivic and sucrose intake following general, mu and kappa opioid antagonists in the hypothalamic paraventricular nucleus of rats. 765 22

Significantly greater inhibition of deprivation-induced food intake occurs following cotreatment with naltrexone and either the D1 antagonist, SCH-23390, the D2 agonist, quinpirole, or the D2 antagonist, haloperidol, relative to naltrexone alone. Cotreatment with the D1 agonist, SKF-38393, failed to alter naltrexone's inhibition of deprivation-induced intake. The present study evaluated whether each of these D1 and D2 agonists and antagonists altered hyperphagia following 2-deoxy-D-glucose (2DG) themselves or in combination with naltrexone. Neither SKF-38393 (1-10 mg/kg) nor SCH-23390 (25-200 micrograms/kg) altered 2DG hyperphagia. Quinpirole (0.025-0.5 mg/kg) dose dependently decreased 2DG hyperphagia. 2DG hyperphagia was respectively increased and decreased by low (50 micrograms/kg) and high (500 micrograms/kg) doses of haloperidol. Cotreatment of SKF-38393 (0.1-1 mg/kg) and naltrexone potently enhanced the inhibition of 2DG hyperphagia relative to naltrexone alone. In contrast, cotreatment of naltrexone and either SCH-23390 (100-200 micrograms/kg) or quinpirole (0.025-0.05 mg/kg) inhibited 2DG hyperphagia in a manner similar to that of naltrexone alone. Finally, cotreatment of haloperidol (5-50 micrograms/kg) and naltrexone transiently enhanced the inhibition of 2DG hyperphagia relative to naltrexone alone.
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PMID:Naltrexone, dopamine receptor agonists and antagonists, and food intake in rats: 2. 2-deoxy-D-glucose. 781 75

Two hypotheses have attempted to account for the abilities of opioid agonists and antagonists to respectively stimulate and inhibit food intake in rats. The first suggests that the opioid system selectively modulates fat intake, while the second suggest that the opioid system selectively alters intake of that macronutrient which the animal prefers. The present study evaluated these two hypotheses by examining total intake and individual macronutrient intake in either food-deprived (24 h) rats or rats made glucoprivic with 2-deoxy-D-glucose (2DG, 200 mg/kg, i.p.) following either vehicle treatment, systemic administration of naltrexone or intracerebroventricular administration of either naltrexone, the mu opioid antagonist, beta-funaltrexamine (B-FNA), the mu1 opioid antagonist, naloxonazine, the kappa opioid antagonist, nor-binaltorphamine (Nor-BNI), the delta opioid antagonist, naltrindole or the delta1 opioid antagonist, DALCE. Systemic administration of naltrexone (0.5-5 mg/kg significantly reduced carbohydrate, fat and total intake in deprived rats, and carbohydrate, fat, protein and total intake in glucoprivic rats. Central administration of naltrexone (5-50 micrograms) significantly reduced fat and total intake in both deprived and glucoprivic rats. B-FNA (5-20 micrograms) significantly reduced carbohydrate, fat and total intake in both deprived and glucoprivic rats Naloxonazine (10-100 micrograms) significantly reduced carbohydrate, fat and total intake in deprived rats, but failed to alter 2DC intake. Nor-BNI (5-20 micrograms) significantly reduced fat and total intake in glucoprivic rats, but failed to alter deprivation intake. Neither naltrindole (20 micrograms) nor DALCE (40 micrograms altered intake in deprived or glucoprivic rats. Carbohydrate or fat preference in deprived rats significantly increased the amount of explained variance in the inhibitory actions of central naltrexone, B-FNA and naloxonazine upon deprivation-induced intake. Carbohydrate or fat preference in glucoprivic rats significantly increased the amount of explained variance in the inhibitory action of systemic and central naltrexone, B-FNA, naloxonazine and Nor-BN upon 2-DG hyperphagia. These data are discussed in terms of the contentions that opioids either selectively alter fat intake pe se or selectively alter the preferred macronutrient.
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PMID:Selective alterations in macronutrient intake of food-deprived or glucoprivic rats by centrally-administered opioid receptor subtype antagonists in rats. 782 Jun 18

Intracerebroventricular neuropeptide Y (NPY) administration to normal rats for 7 days produced a sustained, threefold increase in food intake, resulting in a body weight gain of more than 40 g. Basal plasma insulin and triglyceride levels were increased in NPY-treated compared to vehicle-infused rats by about four- and two-fold, respectively. The glucose utilization index of white adipose tissue, measured by the labelled 2-deoxy-D-glucose technique was four times higher in NPY-treated rats compared to controls. This change was accompanied by an increase in the insulin responsive glucose transporter protein (GLUT 4). In marked contrast, muscle glucose utilization was decreased in NPY-treated compared to vehicle-infused animals. This change was accompanied by an increase in triglyceride content. When NPY-treated rats were prevented from overeating, there was no decrease in muscle glucose uptake, nor was there an increase in muscle triglyceride content. This suggests that muscle insulin resistance of ad libitum-fed NPY-treated rats is due to a glucose-fatty acid (Randle) cycle. When intracerebroventricular NPY administration was stopped and rats kept without any treatment for 7 additional days, all the abnormalities brought about by the neuropeptide were normalized. A tonic central effect of NPY is therefore needed to elicit and maintain most of the hormonal and metabolic abnormalities observed in the present study. Such abnormalities are analogous to those seen in the dynamic phase of obesity syndromes in which high hypothalamic NPY levels have been reported.
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PMID:Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats. 789 49

The effects of repeated treatment with the metabolic stressor 2-deoxy-D-glucose (2-DG: 500 mg/kg/day, 7 days) upon some ingestive and psychological behaviours were investigated, and compared with those elicited by repeated immobilization or cold exposure (2 hr/day, 7 days). Because all these stressors affect central serotonergic systems, 5-HT1A and 5-HT2A receptor-mediated behaviours were also analysed. Both 2-DG administration and immobilization decreased daily food intakes and increased the weight of the adrenals, while all stressors reduced body weight gain. In addition, 2-DG triggered hyperphagia (and reduced body weight loss) throughout the 7 light phases, and hypophagia (and reduced body weight gain) throughout the 7 dark phases. However, the other stressors had only temporary effects during the light phases. These results suggested that immobilized and cold exposed rats, but not 2-DG-treated rats had progressively adapted to their stressors. Furthermore, 2-DG-treated rats exhibited decreased ambulation when placed in the open field, but no change in social interaction. Forepaw treading and flat body posture responses to the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) were not altered by the stressors, but both of them slightly amplified 8-OH-DPAT-induced hypothermia. This change was associated with a decreased head shake response to the 5-HT2A agonist 1-(4-iodo-2,5-dimethoxy-phenyl)-2-aminopropane (DOI) in 2-DG-treated rats, compared with that measured in the other groups. This study opens the possibility that alterations in feeding rhythms has functional consequences on 5-HT2A receptors.
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PMID:Effects of repeated 2-deoxy-D-glucose administration on ingestive, psychological, and 5-HT-related behaviours in the rat. 793 5


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