scholarly journals Effect of glucose on carbohydrate synthesis from alanine or lactate in hepatocytes from starved rats

1980 ◽  
Vol 192 (1) ◽  
pp. 377-380 ◽  
Author(s):  
K Solanki ◽  
F Nyfeler ◽  
U K Moser ◽  
P Walter
Keyword(s):  
Inhibitory Effect ◽  
Label Free ◽  
Carbohydrate Synthesis ◽  
No Inhibition ◽  
Effect Of Glucose ◽  
Substrate Addition

In hepatocytes from starved rats, 10mM-glucose suppressed in incorporation of 2mM labelled alanine into glucose+glycogen by more than 40%, whereas no inhibition was observed with labelled lactate as substrate. Addition of glycerol instead of glucose did not show this inhibition. The inhibitory effect could also be demonstrated in label-free experiments.

Inhibitory effect of phenelzine on oxidative microsomal enzyme systems of rat liver

1983 ◽  
Vol 61 (5) ◽  
pp. 524-529 ◽  
Author(s):  
P. M. Bélanger ◽  
A. Atitsé-Gbeassor
Keyword(s):  
Rat Liver ◽  
Apparent Volume ◽  
Inhibitory Effect ◽  
Volume Of Distribution ◽  
Inhibitory Effects ◽  
Oxidative Reactions ◽  
Total Body ◽  
Apparent Volume Of Distribution ◽  
Cytochrome P 450 ◽  
Substrate Addition

The inhibitory effects of phenelzine on the hepatic microsomal demethylation of aminopyrine, N,N-dimethylaniline, and p-nitroanisole on the hydroxylation of aniline and on the pharmacokinetics of antipyrine were investigated in the rat. Phenelzine produced a competitive and noncompetitive inhibition of the demethylation of p-nitroanisole and N,N-dimethylaniline, respectively, but was a mixed-type inhibitor of the aminopyrine N-demethylase and aniline hydroxylase. The inhibition constant, Ki, varied between 0.06 to 0.25 mM depending on the substrate used. Preincubation of phenelzine for 30 min with the microsomal homogenate prior to substrate addition doubled its inhibitory effect. Phenelzine induced a type II spectral change when combined with oxidized cytochrome P-450 with a Ks value of 0.4 mM. The administration of one dose of 50 mg∙kg−1 of phenelzine sulfate concomitantly with 50 mg∙kg−1 of antipyrine resulted in a significant decrease of the serum elimination of antipyrine. The serum half-life, apparent volume of distribution, and total body clearance of antipyrine were modified to 3.6 h, 294.1 mL∙kg−1, and 56.8 mL∙h−1∙kg−1, respectively, from 1.5 h, 666.7 mL∙kg−1, and 312.5 mL∙h−1∙kg−1 when antipyrine was administered alone. It is concluded that the inhibitory effect of phenelzine on the microsomal oxidative reactions of rat liver is related to its interaction with cytochrome P-450.

scholarly journals Fungicidal Activity of Recombinant Javanicin against Cryptococcus neoformans Is Associated with Intracellular Target(s) Involved in Carbohydrate and Energy Metabolic Processes

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 7011
Author(s):  
Santhasiri Orrapin ◽  
Sittiruk Roytrakul ◽  
Narumon Phaonakrop ◽  
Siriwan Thaisakun ◽  
Khajornsak Tragoolpua ◽  
...  
Keyword(s):  
Cryptococcus Neoformans ◽  
Laser Scanning ◽  
Antifungal Agents ◽  
Biological Activities ◽  
Microscopic Analysis ◽  
Inhibitory Effect ◽  
Antifungal Drugs ◽  
Confocal Laser ◽  
Label Free ◽  
Glycolysis Pathway

The occurrence of Cryptococcus neoformans, the human fungal pathogen that primarily infects immunocompromised individuals, has been progressing at an alarming rate. The increased incidence of infection of C. neoformans with antifungal drugs resistance has become a global concern. Potential antifungal agents with extremely low toxicity are urgently needed. Herein, the biological activities of recombinant javanicin (r-javanicin) against C. neoformans were evaluated. A time-killing assay was performed and both concentration- and time-dependent antifungal activity of r-javanicin were indicated. The inhibitory effect of the peptide was initially observed at 4 h post-treatment and ultimately eradicated within 36 to 48 h. Fungal outer surface alteration was characterized by the scanning electron microscope (SEM) whereas a negligible change with slight shrinkage of external morphology was observed in r-javanicin treated cells. Confocal laser scanning microscopic analysis implied that the target(s) of r-javanicin is conceivably resided in the cell thereby allowing the peptide to penetrate across the membrane and accumulate throughout the fungal body. Finally, cryptococcal cells coped with r-javanicin were preliminarily investigated using label-free mass spectrometry-based proteomics. Combined with microscopic and proteomics analysis, it was clearly elucidated the peptide localized in the intracellular compartment where carbohydrate metabolism and energy production associated with glycolysis pathway and mitochondrial respiration, respectively, were principally interfered. Overall, r-javanicin would be an alternative candidate for further development of antifungal agents.

Activation of members of the mitogen-activated protein kinase family by glucose in endothelial cells

2000 ◽  
Vol 279 (4) ◽  
pp. E782-E790 ◽  
Author(s):  
Wenli Liu ◽  
Aaron Schoenkerman ◽  
William L. Lowe
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Molecular Mechanisms ◽  
Normal Growth ◽  
Inhibitory Effect ◽  
Mitogen Activated Protein Kinase ◽  
P38 Kinase ◽  
Hexosamine Pathway ◽  
Mitogen Activated Protein ◽  
Effect Of Glucose

To better understand the molecular mechanisms for hyperglycemia-induced proatherogenic changes in endothelial cells, the effect of high glucose on activation of members of the mitogen-activated protein kinase (MAPK) family, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK)-1, -2, and -5, and p38 kinase, was examined in bovine pulmonary artery endothelial cells (PAEC). Glucose, fructose, and raffinose induced a concentration-dependent decrease in PAEC growth. Addition of 25 mM glucose, fructose, or raffinose to normal growth medium stimulated an approximately twofold increase in JNK1 activity that was maximal after 24 h, whereas only glucose markedly increased ERK5 activity. Neither ERK1/2 nor p38 kinase activity was increased by glucose, fructose, or raffinose. The antioxidant N-acetylcysteine partially abrogated the glucose-induced increase in ERK5 activity but had no effect on the increase in JNK1 activity. In contrast, azaserine, which prevents increased flux through the hexosamine pathway, decreased glucose-induced JNK1 activity but had no effect on fructose- or raffinose-induced JNK1 activity. Consistent with this finding, glucosamine stimulated a 2.4-fold increase in JNK1 activity and reproduced the inhibitory effect of glucose on PAEC growth. In summary, glucose activates different members of the MAPK family in PAEC via distinct mechanisms. Moreover, the correlation between the ability of different sugars to activate JNK1 and inhibit cell growth suggests that activation of this signaling pathway may contribute to the growth inhibitory effect of glucose in endothelial cells.

scholarly journals Inorganic Phosphate Induces Spore Morphogenesis and Enterotoxin Production in the Intestinal Pathogen Clostridium perfringens

2006 ◽  
Vol 74 (6) ◽  
pp. 3651-3656 ◽  
Author(s):  
Valeria A. Philippe ◽  
Marcelo B. Méndez ◽  
I-Hsiu Huang ◽  
Lelia M. Orsaria ◽  
Mahfuzur R. Sarker ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Inorganic Phosphate ◽  
Food Poisoning ◽  
Inhibitory Effect ◽  
Physiological Signal ◽  
Food Borne ◽  
Intestinal Pathogen ◽  
Important Virulence Factor ◽  
Dna Partitioning ◽  
Effect Of Glucose

ABSTRACT Clostridium perfringens enterotoxin (CPE) is an important virulence factor for food poisoning and non-food borne gastrointestinal (GI) diseases. Although CPE production is strongly regulated by sporulation, the nature of the signal(s) triggering sporulation remains unknown. Here, we demonstrated that inorganic phosphate (Pi), and not pH, constitutes an environmental signal inducing sporulation and CPE synthesis. In the absence of Pi-supplementation, C. perfringens displayed a spo0A phenotype, i.e., absence of polar septation and DNA partitioning in cells that reached the stationary phase of growth. These results received support from our Northern blot analyses which demonstrated that Pi was able to counteract the inhibitory effect of glucose at the onset of sporulation and induced spo0A expression, indicating that Pi acts as a key signal triggering spore morphogenesis. In addition to being the first study reporting the nature of a physiological signal triggering sporulation in clostridia, these findings have relevance for the development of antisporulation drugs to prevent or treat CPE-mediated GI diseases in humans.

Nutrient feedback inhibition of gastric emptying plays a larger role than osmotically dependent duodenal resistance

1993 ◽  
Vol 265 (4) ◽  
pp. G672-G676
Author(s):  
H. C. Lin ◽  
J. D. Elashoff ◽  
Y. G. Gu ◽  
J. H. Meyer
Keyword(s):  
Gastric Emptying ◽  
Analysis Of Variance ◽  
Feedback Inhibition ◽  
Inhibitory Effect ◽  
Duodenal Fistula ◽  
Inhibitory Feedback ◽  
Specific Feedback ◽  
Hyperosmolar Solutions ◽  
Effect Of Glucose ◽  
Hyperosmolar Glucose

The slowing of gastric emptying by hyperosmolar solutions has been postulated to result from the triggering of duodenal osmoreceptor feedback on the stomach. We tested the idea that the inhibition of gastric emptying by a hyperosmolar solution depended on the duodenal resistance and the triggering of nutrient-specific feedback by tracking gastric emptying of 300 and 1,200 mosmol/kgH2O test solutions in 12 dogs in which duodenal resistance was either removed (by temporarily diverting chyme from uncorked duodenal fistula) or preserved (by keeping duodenal fistula corked). Mannitol was used to test osmolality alone, and glucose was used to examine the combined effects of osmolality and nutrient-specific inhibitory feedback. We found that: 1) the slowing effect of hyperosmolality was more marked with the duodenal resistance preserved (P < 0.05; analysis of variance), 2) the slowing effect of glucose was greater than that of mannitol for all conditions (P = 0.01; analysis of variance), and 3) the inhibitory effect of mannitol was localized to the duodenum. We conclude that inhibition of gastric emptying by hyperosmolar mannitol depended primarily on duodenal resistance, while the inhibitory effect of hyperosmolar glucose depended on nutrient-specific feedback on the stomach more than duodenal resistance.

Conditions Affecting the Inhibitory Action of RLP on Radiation Leukaemogenesis in Mice

1967 ◽  
Vol 53 (1) ◽  
pp. 5-17 ◽  
Author(s):  
I. Bekenblum ◽  
N. Trainin ◽  
G. Cividalli ◽  
Louise Boiato-Chen ◽  
Ahuva Knyszynski
Keyword(s):  
Inhibitory Action ◽  
Radiation Effect ◽  
Radiation Treatment ◽  
Inhibitory Effect ◽  
Myelogenous Leukaemia ◽  
Cell Free Extract ◽  
No Inhibition ◽  
A Cell ◽  
Akr Mice ◽  
Optimal Effect

The inhibitory effect of RLP (a cell-free extract derived from sheep spleen) on radiation leukaemogenesis in mice, was studied under different biological conditions, in order to determine the limitations and specificity of its action. For inhibition of radiation leukaemogenesis (lymphatic, thymic, type) in C57BL/6/Jax mice, the RLP injections were required to be given repeatedly — at least 4 times for demonstrable effect, and 10 times for optimal effect — the treatment begun about 1 hour after irradiation. Weaker effects were obtained when the treatment was begun 24 hours after irradiation, and no inhibition when the injections were given before the start of the radiation treatment, or begun 2 weeks after its completion. In irradiated RF mice, RLP inhibited the induction of lymphatic (thymic) leukaemia, while that of myelogenous leukaemia appeared to be augmented. RLP failed to inhibit the spontaneous development of the lymphatic (thymic) leukaemia in AKR mice. The results support the conclusion that the inhibitory action of RLP is an anti-radiation effect with respect to leukaemogenesis, rather than an antagonism against the leukaemogenic process proper.

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