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)

We found previously that the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) significantly reduced 2-deoxy-D-glucose (2-DG)-induced hyperphagia in rats. To clarify the involvement of 5-HT, we investigated the effects of 5-HT receptor antagonists on inhibitory effects of L-NAME on 2-DG-induced hyperphagia. The effects of L-NAME on 2-DG-induced hyperphagia were inhibited by the 5-HT1B receptor antagonist metergoline. However, the 5-HT2 receptor antagonist ritanserin had no such effect. These results suggest that the anorectic effects of L-NAME may be related to serotonergic mechanisms.
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PMID:The involvement of 5-HT1B receptors in the inhibitory effects of nitric oxide synthase inhibitor on 2-deoxy-D-glucose-induced hyperphagia in rats. 929 9

Opioid receptor subtype antagonists differentially alter food intake under deprivation (24 h), glucoprivic (2-deoxy-D-glucose, 500 mg/kg, i.p.) or palatable (10% sucrose) conditions with mu (beta-funaltrexamine) and kappa (nor-binaltorphamine), but not delta1 ([D-Ala2,Leu5,Cys6]enkephalin) opioid antagonists reducing each form of intake following ventricular microinjection. Both mu and kappa opioid antagonists microinjected into either the hypothalamic paraventricular nucleus or the nucleus accumbens reduce intake under deprivation and glucoprivic conditions. Palatable intake is reduced by both antagonists in the paraventricular nucleus, but only mu antagonists are active in the accumbens. Food intake is stimulated by mu and delta, but not kappa, opioid agonists microinjected into the ventral tegmental area. The present study examined whether food intake under either deprivation, glucoprivic or palatable conditions was altered by bilateral administration of general (naltrexone), mu, kappa, delta1 or delta2 (naltrindole isothiocyanate) opioid antagonists into the ventral tegmental area. Deprivation (24 h)-induced feeding was significantly reduced by high (50 microg), but not lower (10-20 microg) doses of naltrexone (21%), and by delta2 (4 microg, 19%) antagonism in the ventral tegmental area. 2-Deoxy-D-glucose (500 mg/kg, i.p.)-induced hyperphagia was significantly reduced by high (50 microg), but not lower (20 microg) doses of naltrexone (64%), and by delta2 (4 microg, 27%) antagonism in the ventral tegmental area. Sucrose (10%) intake was significantly reduced by naltrexone (20-50 microg, 25-39%) and delta2 (4 microg, 25%) antagonism in the ventral tegmental area. Neither mu, kappa nor delta1 antagonists were effective in reducing any form of intake following microinjection into the ventral tegmental area. These data indicate that the ventral tegmental area plays a relatively minor role in the elicitation of these forms of food intake, and that delta2, rather than mu, kappa or delta1 opioid receptors appear responsible for mediation of these forms of intake by this nucleus.
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PMID:Evaluation of opioid receptor subtype antagonist effects in the ventral tegmental area upon food intake under deprivation, glucoprivic and palatable conditions. 936 10

Effects of adrenalectomy on the 5-HT1A receptor agonist 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT)- and 2-deoxy-D-glucose (2-DG)-induced hyperphagia were investigated in rats. Prior adrenalectomy completely inhibited 2-DG-induced hyperphagia, although it did not affect increases in food intake elicited by 8-OH-DPAT. These results suggest that 8-OH-DPAT-induced hyperphagia is independent of the adrenal hormone, corticosterone while 2-DG-induced hyperphagia is closely related to corticosterone.
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PMID:Effects of adrenalectomy on hyperphagia induced by the 5-HT1A receptor agonist 8-OH-DPAT and 2-deoxy-D-glucose in rats. 966 10

Possible involvement of nitric oxide (NO) in glucoprivic hyperphagia was investigated in nondeprived male ICR mice in independent groups designs. One pair of experiments demonstrated dose-related reductions in 2-deoxy-D-glucose (2DG)- and insulin-induced solid food intake with increasing dose (10, 25, and 50 mg/kg s.c.) of the NO-synthase (NOS) inhibitor, NG-nitro-L-arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle controls. In a second pair of experiments, initial pretreatment with L-arginine (500 and 1000 mg/kg i.p.) partially or completely restored the feeding inhibitory action of an effective challenge dose (25 mg/kg) of L-NOARG; D-arginine (500 mg/kg i.p.) was ineffective, thus supporting a stereospecific action of arginine. A third set of experiments demonstrated dose-related reduction in glucoprivic feeding under delayed access (4 or 6 h) to food. These findings suggest involvement of NO in glucoprivic hyperphagia; they are consistent with and extend research linking NO and ingestive behaviors through use of NOS inhibitors. Deprivation-induced drinking was attenuated by these doses of L-NOARG as well.
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PMID:A nitric oxide synthase inhibitor NG-nitro-L-arginine, attenuates glucoprivic feeding and deprivation-induced drinking in the mouse. 967 42

Dispensing hyperalimentation orders in a timely and correct manner can be demanding for staff pharmacists. Using a computer to calculate the amounts of amino acid, dextrose, and electrolyte solutions can greatly reduce pharmacy response time and insure accuracy in filling the physician's order. This report lists a computer program that will do these calculations and also gives consideration to the technical aspects of using the program.
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PMID:Hyperalimentation order calculations using a computer. 1031 15

Interoreceptors in the central nervous system elicit compensatory behavioral and physiological responses to cellular glucopenia. Antagonism of mu and kappa opioid receptors attenuates glucoprivic hyperphagia, findings that implicate these peptidergic receptors in the central processing of metabolic regulatory signals. Several hypothalamic structures of critical importance for the regulation of energy balance exhibit one or both of these receptors. The following studies investigated the role of these opioid receptors in glucoprivic induction of immediate-early gene expression in these brain sites. Male rats were pretreated with beta-funaltrexamine (mu antagonist), Mr-1452 MS (kappa antagonist), or vehicle prior to intraperitoneal injection of the glucose antimetabolite, 2-deoxy-D-glucose (2DG), then sacrificed by transcardial perfusion 2 h later. Nuclear immunolabeling for the transcription factor, Fos, was observed in several preoptic and hypothalamic sites following 2DG administration. Rats pretreated with the mu antagonist exhibited significantly fewer Fos-positive neurons in the medial preoptic area and dorsomedial hypothalamic nucleus in response to 2DG, compared to vehicle-pretreated controls. Blockade of kappa receptors diminished 2DG and induced Fos staining in the paraventricular and supraoptic nuclei. Numbers of Fos-positive cells in the arcuate nucleus and ventrolateral hypothalamic area were not altered by either antagonist. The present data implicate mu and kappa opioid receptors in neural mechanisms underlying glucoprivic induction of the Fos stimulus-transcription pathway by local neurons in discrete hypothalamic sites.
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PMID:Effects of mu and kappa opioid receptor antagonists on glucoprivic induction of Fos immunoreactivity in the rat preoptic area and hypothalamus. 1043 81

The effects of the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5, 10-imine (MK-801) on 2-deoxy-D-glucose-induced hyperphagia were investigated in rats. MK-801 significantly increased 2-deoxy-D-glucose-elicited eating. The facilitating effects of MK-801 on 2-deoxy-D-glucose-elicited feeding were not affected by coadministration of a nitric oxide (NO) precursor, L-arginine. Because NO synthase inhibitors inhibit 2-deoxy-D-glucose-induced hyperphagia and activation of the NMDA receptor leads to NO formation, our results suggest that blockade of the NMDA receptor increases 2-deoxy-D-glucose-induced hyperphagia, which is unrelated to inhibition of NO, and that NMDA receptors may play a role in satiety.
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PMID:Influence of the non-competitive NMDA receptor antagonist MK-801 on 2-deoxy-D-glucose-induced hyperphagia in rats. 1047 26

The glucostatic theory supports the role of central and peripheral substrate "sensors" in monitoring cellular glucose metabolism. Induction of hyperphagia and hyperglycemia by intracerebroventricular (i.c.v.) delivery of drugs inhibiting glucose uptake or oxidation suggests that glucose "sensors" are accessible from the cerebroventricular system. Although glucopenia elevates neurohypophyseal vasopressin (VP) and oxytocin (OXY) secretion and induces c-fos expression by hypothalamic paraventricular (PVN) and supraoptic (SON) neurons, the origin of glucoprivic regulatory signals impinging upon these cell populations is unclear. The following study evaluated immunolabeling of hypothalamic VP and OXY neurons for the nuclear transcription factor, Fos, following systemic vs. i.c.v. delivery of the glucose antimetabolite, 2-deoxy-D-glucose (2DG). Intraperitoneal drug treatment resulted in Fos expression by a high proportion of AVP- and OXY-ir neurons in the PVN and SON, whereas i.c.v. antimetabolite administration resulted in immunostaining of a smaller proportion of AVP neurons and a lack of colabeling of OXY neurons in both sites. These results suggest that decreased glucose metabolism within the periventricular CNS is a stimulus for central mechanisms that activate the Fos stimulus-transcription cascade in a discrete subpopulation of VP neurons in the PVN and SON. Alternatively, the absence of demonstrable Fos expression by OXY neurons in the same structures suggests that the functional status of these cells is regulated by glucoprivic stimuli of peripheral and/or nonperiventricular central origin.
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PMID:Intraventricular 2-deoxy-D-glucose induces Fos expression by hypothalamic vasopressin, but not oxytocin neurons. 1071 20

Reports that glucose antimetabolite treatment elicits hyperphagia and hyperglycemia suggest that decreased oxidation of this energy substrate elicits compensatory responses that enhance cellular fuel availability. Neurons the lateral hypothalamic area (LHA) synthesize the orectic neuropeptide, orexin-A (ORX-A). The present study evaluated the functional responsiveness of orexinergic neurons to glucopenia by investigating whether these cells express the genomic regulatory protein, Fos, in response to glucoprivation. Adult male rats were sacrificed 2h after i.p. (400 mg/kg) or intracerebroventricular (i.c.v.; 100 microg) administration of the antimetabolite, 2-deoxy-D-glucose (2DG) or saline. Sections through the LHA, from the level of the paraventricular nucleus (PVN) to the posterior hypothalamic area (PHA), were processed by dual-label immunocytochemistry for Fos- and OXY-A-immunoreactivity (-ir). Although orexinergic neurons expressed negligible Fos-ir following vehicle administration, dual-labeled ORX-A neurons were observed in the LHA, as well as the dorsomedial hypothalamic nucleus (DMN) and PHA, in both drug-treated groups. Bilateral cell counts from representative levels of the LHA, DMN, and PHA showed that in each structure, a greater proportion of ORX-A neurons were immunostained for Fos in response to systemic than following i.c.v. treatment with 2DG. These results provide evidence for the transcriptional activation of hypothalamic ORX-A neurons by diminished glucose availability, data that suggest that these cells may function within central pathways that govern adaptive responses to deficits of this substrate fuel. The findings also support the view that a proportion of this phenotypic population is responsive to glucoprivic stimuli of central origin.
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PMID:Hypothalamic orexin-A-immunpositive neurons express Fos in response to central glucopenia. 1123 58

We report a 63-year-old male with central venous catheter-related infection caused by Malassezia sympodialis after total gastrectomy for a gastric cancer. He had fever and his leukocyte counts and C-reactive protein were elevated 14 days after his operation. After his central venous hyperalimentation catheter was removed, the inflammatory signs immediately disappeared, suggesting an intravenous catheter-related infection. A yeast-like fungus was cultured in brain-heart infection semi-solid agar ten days later, and was diagnosed morphologically as Malassezia sp. This strain was identified as M. sympodialis by Tween assimilation test and was confirmed by whole-sequence of internal transcribed spacer 1 regions (ITS1). This is the first report of catheter-related infection caused by M. sympodialis. This strain grew and was subcultured on CHROMagar Candida, potato dextrose agar and Sabouraud agar. There have been no reports of such a lipid-independent Malassezia sp. except for M. pachydermatis. The mechanism of lipid independence of this strain is undetermined and future work is needed. Malassezia sp. is receiving increased attention as an etiologic pathogen of catheter-related fungemia in clinical microbiology laboratories and infectious disease sections.
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PMID:[A Case of central venous catheter-related infection with Malassezia sympodialis]. 1170 51


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