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)

The influence of hepatic branch vagotomy (HBV) in comparison to sham-vagotomy (SV) on the hyperphagia induced in rats by intraperitoneally injected 2-deoxy-D-glucose (2-DG, 250 mg/kg b.wt.) was investigated in nine experiments. Injections were given at various times of the 12-h light/12-h dark cycle in ad libitum fed rats (0 h, 1 h, 2 h, 4 h, 10 h after dark onset; 0 h and 6 h after onset of the bright phase). In two further experiments, 2-DG was injected 1 h after the onset of darkness or at the onset of light immediately after a meal (duration: 30 min) induced by short-term (2 h) food deprivation. 2-DG significantly increased food intake in SV-rats in all experiments, whereas in HBV rats there was no significant response to 2-DG in two experiments (injections 1 h after dark onset after ingestion of a meal, or 4 h after the onset of darkness). These findings indicate that an intact hepatic vagus branch is a prerequisite for "glucoprivic" feeding under certain conditions, and that hepatic vagal glucoreceptors participate in the control of feeding.
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PMID:Circadian effects of hepatic branch vagotomy on the feeding response to 2-deoxy-D-glucose in rats. 812 Mar 41

Seventeen children aged 3 weeks to 19 months with severe Protracted Diarrhea (PD), and who were deteriorating on our standard management protocol (including special diets) were given Parenteral Nutrition (PN) for 4 to 19 days with crystalline aminoacid solution (Vamin N) in 10% dextrose and lipid emulsion (Intralipid 10%). Peripheral lines were used in majority (84%). Enteral feeds were started early and rebuilt as per tolerance. The mean daily protein and caloric intake achieved by hyperalimentation was 2.2 +/- 0.7 g/kg and 106 +/- 41 K cal/kg respectively. Diarrheal control and improvement in nutritional status was achieved in all but 4 who died (2 of refractory diarrhea and 2 of sepsis, 1 of which was probably PN related). Other PN related, treatable complications included thrombophlebitis (11.8%), sepsis (17.6%), and metabolic imbalance (17.6%). PN solutions and accessories alone cost an approximate average of Rs. 280/day, with extras for biochemical monitoring (Rs. 70/day) and special nursing (Rs. 200/day). Only 5 of the 13 survivors had a significant relapse of PD, within 5 to 80 days of discharge, necessitating further PN in 2. There were no further deaths. PN was therefore, found to be of life saving value in 13 of 17 children with severe protracted diarrhea and therefore, must be available in specialised units caring for such children.
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PMID:Parenteral nutrition in the management of severe protracted diarrhea. 824 81

Glucoprivic feeding induced by intraperitoneal (IP) injection of 2-deoxy-D-glucose (2-DG, 250 mg/kg body weight) in the middle of the light phase was investigated in old (age: 15-16 months) and young (age; 2.5-3.5 months) hepatic branch-vagotomized (HBV) and sham-vagotomized (SV) rats. Rats were fed either a carbohydrate-rich diet or a fat-enriched diet with a moderate carbohydrate content. The glucoprivic feeding response was greater in 13-h food-deprived old HBV rats than in 13-h food-deprived old SV rats on both diets. 2-Deoxy-D-glucose produced a greater feeding response when rats were fed the fat-enriched diet. Independent of the diet, the transient hyperphagia induced by 2-DG was followed by a long-term hypophagia in old SV rats, but not in old HBV rats. In 13-h food-deprived young rats, hepatic branch vagotomy did not affect the changes in food intake induced by 2-DG. In undeprived old and young rats, the feeding response to 2-DG, exceeding that of deprived rats, was also not affected by HBV. It is concluded that under certain conditions hepatic branch vagotomy eliminates a 2-DG-induced signal inhibiting food intake and thus enhances glucoprivic feeding. The feeding response to 2-DG therefore seems to depend on stimuli affecting food intake in an antagonistic manner.
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PMID:Hepatic branch vagotomy enhances glucoprivic feeding in food-deprived old rats. 837 18

Cholestatic jaundice is the major complication of total parenteral nutrition (TPN). Both the intravenous (IV) route of nutrition and the enteral fast have been implicated as causes of TPN-associated cholestasis (TPN-AC). The purpose of this study was to determine whether TPN-AC is caused by the TPN solution itself or the IV route of administration and enteral fast. Prepubescent rabbits (n = 24) were divided into four groups: CONTROL, fed standard lab chow; TPN, received a standard hyperalimentation solution of dextrose, Aminosyn, and lipids via the jugular vein; ENT, received the same hyperalimentation solution via a duodenostomy tube; and OSM, received a polymeric formula (Osmolite) via a duodenostomy tube. After 14 days on these diets, we measured bile flow, bile acid excretion, sulfobromophthalein (BSP) excretion, plasma amino acid profile, serum liver enzymes, and liver histology. Statistical analysis was by analysis of variance. Hyperalimentation solution significantly depressed hepatobiliary function, whether it was given IV or by gut. Bile flow in both the TPN (36.4 microL/kg/min) and ENT (46.2) groups was significantly less than CONTROL (84.5) or OSM (62.9). Hepatic secretory function, measured by excretion of the cholephilic dye BSP, was depressed in both TPN and ENT (57% and 55% of IV dose excreted in bile over 60 minutes, respectively) compared with CONTROL (84%) or OSM (71%). Serum liver enzymes were normal in all groups. Histological injury similar to TPN-AC in humans (portal inflammation and hepatocyte degeneration) was seen in both groups receiving the hyperalimentation solution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatobiliary dysfunction during total parenteral nutrition is caused by infusate, not the route of administration. 846 53

Ventricular microinjection studies found that whereas mu (beta-funaltrexamine, B-FNA), mu1 (naloxonazine) and kappa (nor-binaltorphamine, Nor-BNI) opioid receptor antagonists, but not delta antagonists, reduce deprivation-induced intake, kappa and mu, but not mu1 or delta antagonists reduce both 2-deoxy-D-glucose (2DG) hyperphagia and sucrose intake. Since opioid agonists stimulate spontaneous food intake in the accumbens, the present study examined whether administration of either naltrexone, B-FNA or Nor-BNI in the accumbens altered intake under deprivation (24 h), glucoprivic (2DG: 500 mg/kg, i.p.) or palatable sucrose (10%) conditions. Naloxonazine's effects in the accumbens were also evaluated for deprivation-induced intake. Deprivation-induced intake was significantly decreased over 4 h by naltrexone (5-20 micrograms, 44%), B-FNA (1-4 micrograms, 55%) and Nor-BNI (4 micrograms, 31%) but not naloxonazine (10 micrograms) in the accumbens. 2DG hyperphagia was significantly decreased by naltrexone (10-20 microgram, 79%), B-FNA (1-4 micrograms, 100%) and NOR-BNI (104 micrograms, 75%) in the accumbens. Sucrose intake was significantly decreased by naltrexone (50 micrograms, 27%) and B-FNA (1-4 micrograms, 37%), but not NOR-BNI in the accumbens. These data suggest that mu receptors, and particularly the mu2 binding site in the accumbens are responsible for the opioid modulation of these forms of intake in this nucleus, and that this control may be acting upon the amount of intake per se.
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PMID:General, mu and kappa opioid antagonists in the nucleus accumbens alter food intake under deprivation, glucoprivic and palatable conditions. 862 11

The role of beta-adrenoreceptors in modulating feeding in glucoprivation- and lipoprivation-induced hyperphagias was studied in rats by measuring the efficacy of the selective beta2-adrenoreceptor agonist salbutamol to antagonize the hyperphagic response induced by injection of 2-deoxy-D-glucose (2-DG), insulin, or sodium mercaptoacetate (MA). 2-DG and insulin are blockers of glucose utilization, and their administration stimulates receptor cells that are selectively sensitive to central glucose availability. MA stimulates feeding in rats maintained on a fat-supplemented diet, by blocking fatty acid oxidation at different levels in the metabolic pathway. We found that salbutamol dose-dependently antagonized both the insulin- and MA-induced hyperphagia, with reductions in food intake up to 100% compared with rats treated with insulin or MA alone. On the contrary, salbutamol, even at the highest dose (15 mg/kg, IP), was completely ineffective against 2-DG-induced hyperphagia. The present results support the previously proposed notion that there are different neuronal or humoral circuits underlying the hyperphagic responses to the metabolic stimuli induced by glucoprivation (i.e., 2-DG and insulin administration), and they extend our knowledge on the effects of salbutamol on glucoprivic and lipoprivic control of feeding.
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PMID:Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia. 874 3

MOR-1 encodes a mu receptor. In an effort to establish the relationship of this cloned opioid receptor with ingestive behavior and analgesia in rats, the present study examined the actions of four antisense oligodeoxynucleotides aimed at exons 1 (AS1), 2 (AS2), 3 (AS3) and 4 (AS4) of the MOR-1 clone, as well as a mismatch antisense sequence (MS1). Rats were administered intracerebroventricular injections (10 micrograms/2 microliters) of each of the oligodeoxynucleotides on days 1, 3 and 5. Body weight and spontaneous food and water intake were monitored daily. In addition, 2-deoxy-D-glucose (2DG)-induced hyperphagia, central Angiotensin II (ANG-II) induced hyperdipsia and central morphine analgesia were examined 24 h following the last antisense injection. AS1, AS2, AS3 and AS4 each significantly reduced body weight (7-17 g), food intake (8-13 g) and water intake (11-23 ml), while the vehicle or MS1 conditions significantly increased weight (9-20 g) and produced smaller reductions (2-4 g) in food intake. None of the AS probes altered the magnitude of either 2DG-induced hyperphagia or ANG-II-induced hyperdipsia. Central morphine analgesia was reduced by pretreatment with AS1 and AS4, but not AS2, AS3 or MS1. The sensitivity of general feeding to all four exons suggest that the receptor responsible for this action is encoded by the MOR-1 clone. The differences between feeding and morphine analgesia raise the possibility that these two actions are mediated through different mu receptor subtypes. Our results also demonstrate the viability of the in vivo antisense technique in modulating opioid-mediated ingestive responses.
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PMID:Antisense oligodeoxynucleotides against the MOR-1 clone alter weight and ingestive responses in rats. 878 66

Peripherally administered, the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), significantly suppressed the food intake of food-deprived rats. alpha-Methyl-5-HT also inhibited 2-deoxy-D-glucose-induced hyperphagia in rats. The alpha-methyl-5-HT-induced hypophagia was antagonized by the 5-HT2A receptor antagonist, ketanserin. The alpha-methyl-5-HT-induced decrease in food intake of food-deprived rats was not inhibited by prior adrenodemedullation. The peripheral 5-HT3 receptor agonist, 2-methyl-5-HT, did not affect food intake in food-deprived or 2-deoxy-D-glucose-treated rats. These results suggest that the peripheral 5-HT2A receptor may participate in the regulation of food intake and that its hypophagic effects are not associated with its adrenaline-releasing effects from the adrenal gland. Lastly, the peripheral 5-HT3 receptor did not participate in feeding control.
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PMID:Effects of peripheral 5-HT2 and 5-HT3 receptor agonists on food intake in food-deprived and 2-deoxy-D-glucose-treated rats. 898 44

Delta and kappa opioid receptors have been differentiated into further subtypes based upon both biochemical and pharmacological analgesic assays. Whereas hyperphagia elicited by the kappa1 receptor agonist, U50488H is blocked by general and kappa1 opioid antagonists, hyperphagia elicited by the kappa3 receptor agonist, naloxone benzoylhydrazone (NalBzOH) is blocked by general, but not kappa1 opioid antagonists. The first study assessed the opioid antagonist profile of hyperphagia elicited by centrally administered delta1 ([D-Pen2, D-Pen5]-enkephalin, DPDPE: 5-50 microg) and delta2 ([D-Ala2, Glu4]-Deltorphin, Delt II: 5-50 microg) agonists following central pretreatment with general (naltrexone), delta1 ([D-Ala2, Leu5, Cys6]-enkephalin, DALCE) and delta2 (naltrindole isothiocyanate, NTII) opioid antagonists. It is also important to determine whether selective opioid receptor subtype agonists are capable of altering intake in ingestive situations other than spontaneous feeding. The second study examined whether centrally administered delta1, delta2, kappa1 or kappa3 agonists altered the pattern and magnitude of hyperphagia elicited by 2-deoxy-D-glucose (2DG: 50-400 mg/kg, IP). DPDPE-induced hyperphagia was significantly reduced by naltrexone and NTII, but not DALCE. Delt II-induced hyperphagia was significantly reduced by DALCE and NTII, but not naltrexone. Pairing Delt II (5 microg) with low (100-200 mg/kg) 2DG doses significantly enhanced intake, producing a leftward (3-fold) shift in 2DG's hyperphagic dose-response curve. In contrast, DPDPE failed to alter 2DG-induced hyperphagia, and kappa1 and kappa3 opioid agonists each produced small, but significant increases in 2DG-induced hyperphagia. The antagonist data suggest the possibility of physiological and pharmacological interactions between delta receptor subtypes in mediating food intake, and it would appear that delta2 opioid receptors exert facilitatory effects upon glucoprivic hyperphagia.
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PMID:Delta and kappa opioid receptor subtypes and ingestion: antagonist and glucoprivic effects. 907 69

The effects of a nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on 2-deoxy-D-glucose (2-DG)-induced hyperphagia were investigated in rats. L-NAME dose-dependently inhibited 2-DG-induced eating in non-food-deprived rats, although the inactive isomer D-NAME on 2-DG-induced hyperphagia were inhibited by co-administration of L-arginine. The neuronal NO synthase inhibitor 7-nitroindazole also inhibited 2-DG-induced hyperphagia. These results suggest that 2-DG-induced hyperphagia is linked with NO and that brain NO may participate in this hyperphagic model.
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PMID:Involvement of nitric oxide in 2-deoxy-D-glucose-induced hyperphagia in rats. 924 91


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