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)

Hyperammonemic encephalopathy has occasionally been reported in uremic patients receiving hyperalimentation with essential amino acid (EAA) as a source of nitrogen as one of the remaining treatment options when the enteric routes were prohibited. We encountered this complication in a patient with normal renal function. A rat animal model was designed to elucidate the mechanism of hyperammonemia resulting from hyperalimentation with EAA as a source of nitrogen. Sixty-four male Long-Evan rats were divided into eight groups receiving feeds ad libitum or different formula of hyperalimentation. Hyperammonemia was found in every rat given hyperalimentation with EAA as the only nitrogen source. Using the Tukey honestly significant difference test, the results were significantly higher (p < 0.001) than that of the control group which were given feeds ad libitum and those groups given hyperalimentation for the same number of days but with mixed amino acid (MAA) as the nitrogen source. Adding arginine to EAA for a further four days after initial administration of EAA hyperalimentation for three days only slightly lowered the mean serum ammonia level. When compared to that of the three-day EAA hyperalimentation group, the difference was not statistically significant. Adding arginine, citrulline, and ornithine to EAA for a further four days significantly lowered the mean serum ammonia level. When we changed EAA hyperalimentation to MAA hyperalimentation for a further four days, the mean serum ammonia level decreased dramatically to nearly normal. Hyperalimentation using EAA as the exclusive source of nitrogen resulted in hyperammonemia. A deficiency of arginine or other amino acids of the urea cycle failed to account completely for the hyperammonemia observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperammonemic encephalopathy due to essential amino acid hyperalimentation. 785 37

Persistent pulmonary hypertension of the newborn (PPHN) is a life-threatening disorder of neonates manifested by vasoconstriction of the pulmonary arteries. Recently, the gas nitric oxide (NO) has been used with some success in the management of infants with PPHN. Exogenous administration of NO selectively dilates the pulmonary vascular bed. NO is naturally synthesized in the body from the amino acid L-arginine. Here we report our findings that infants with PPHN are deficient in arginine and achieve normal or elevated plasma arginine concentrations with intravenous hyperalimentation. We prospectively identified and studied 10 infants with PPHN who were not receiving protein or amino acids for at least 24 h and compared their plasma arginine concentrations to 8 control infants without PPHN given similar nutrition. Plasma arginine concentrations were 32 +/- 14 and 52 +/- 20 mumol/l in infants with PPHN and control infants, respectively (p = 0.02). There were no other statistically significant differences in plasma amino acid concentration for any of the 22 other amino acids determined. Infants with PPHN who were subsequently treated with amino acid infusions had plasma arginine concentrations of 115 +/- 48 mumol/l (mean of ten determinations at 86 +/- 27 h after initiation of intravenous amino acids in five PPHN infants).
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PMID:Arginine deficiency accompanies persistent pulmonary hypertension of the newborn. 799 49

The presence of a nitric oxide synthetase (NOS) was demonstrated in the rat brain. It has been demonstrated recently that NOS-inhibitors reduce food intake in mammals and this suggest that nitric oxide (NO) might be a physiological mediator involved in the mechanisms controlling feeding behavior. Actually, there is no information about the acute central and peripheral effects of NOS-inhibitors on feeding behavior in obese and lean Zucker rats. That is why we investigated the acute dose-dependent activity of NG-Nitro-Arginine-Methyl-Ester (L-NAME) on food intake and feeding behavior in these rats. When given peripherally in the obese rats, L-NAME produced a dose-dependent decrease in food intake (p<0.001). The calculated MED and the ED 50 were 0.50 mg/kg IP and 3.46 mg/kg IP, respectively. These effects could not be reproduced in the lean Zucker rats whatever the dose used (p=0.59). The anorectic properties of L-NAME were very well translated into the microstructure of the feeding behavior. Time spent to eat (p<0.001), meal duration (p<0.01) and meal number (p<0.01) were reduced in the obese rats. Interestingly, L-NAME produced the same effects in the lean rats, but meal size increased in a compensatory manner. Central administration of L-NAME reproduced the same effects in the obese rats, but lean rats still remained insensitive. Central aminergic and/or peptidergic defects associated with the expression of hyperphagia might explain the differences observed between these lean and the obese animals. These results indicate a role of nitric oxide in the expression of hyperphagia and show that it might be a physiological mediator involved in the mechanisms controlling feeding behavior.
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PMID:Nitric oxide mediates hyperphagia of obese Zucker rats: relation to specific changes in the microstructure of feeding behavior. 862 5

Two experiments investigated a possible role of nitric oxide (NO) in chlordiazepoxide (CP)-induced feeding in nondeprived male ICR mice in independent groups designs. Experiment 1 demonstrated a dose-related decrease in CP-induced solid food intake over a 60-min test period with increasing dose (10, 25, and 50 mg/ kg SC) of the NO-synthase (NOS) inhibitor, L-NG-nitro arginine (L-NOARG), reaching statistical significance at 10 mg/kg L-NOARG when compared to vehicle control. Identical doses of L-NOARG failed to significantly affect normal feeding in vehicle treated mice. In Experiment 2, initial pretreatment with L-arginine (500 and 1000 mg/kg IP) partially or completely restored the feeding inhibitory action of a challenge dose (25 mg/kg SC) of L-NOARG; D-arginine (500 mg/kg IP) was ineffective, thus supporting a stereospecific action of arginine. Arginine isomers did not differentially affect intake in normal feeding animals. These results implicate involvement of NO in CP-induced hyperphagia; they are consistent with and extend research linking NO and ingestive behaviors.
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PMID:Possible involvement of nitric oxide in chlordiazepoxide-induced feeding in the mouse. 895 73

We investigated nitric oxide (NO) involvement in the hyperphagia induced by the 5-HT1A receptor agonist 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT). A NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), dose dependently inhibited 8-OH-DPAT-induced eating in freely feeding rats. However, the inactive isomer D-NAME was without effect. The inhibitory effects of L-NAME on 8-OH-DPAT-induced hyperphagia were reversed by simultaneous administration of L-arginine. These results suggest that NO participates in the 8-OH-DPAT-induced hyperphagia which is elicited by activation of the 5-HT1A receptor.
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PMID:Effects of a nitric oxide synthase inhibitor on 5-HT1A receptor agonist 8-OH-DPAT-induced hyperphagia in rats. 898 45

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

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

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

The effects of the neuronal nitric oxide (NO) synthase inhibitor 7-nitroindazole on 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT)-induced hyperphagia, which is mediated by the 5-HT1A autoreceptor, were investigated in rats. 7-Nitroindazole suppressed 8-OH-DPAT-elicited increases in food intake. The inhibitory effects of 7-nitroindazole on 8-OH-DPAT-induced feeding were prevented by the NO precursor L-arginine. Although 8-OH-DPAT decreases 5-hydroxytryptamine (5-HT) synthesis, 7-nitroindazole did not reverse the 8-OH-DPAT-elicited decrease in 5-HT synthesis. Therefore, these results indicate that NO formed in the brain is involved in 8-OH-DPAT-induced hyperphagia and that the hypophagic effects of 7-nitroindazole are not dependent on 5-HT synthesis.
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PMID:A neuronal nitric oxide synthase inhibitor 7-nitroindazole reduces the 5-HT1A receptor against 8-OH-DPAT-elicited hyperphagia in rats. 1044 82

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


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