Ochratoxin A induces reprogramming of glucose metabolism by switching energy metabolism from oxidative phosphorylation to glycolysis in human gastric epithelium GES-1 cells in vitro

2020 ◽  
Vol 333 ◽  
pp. 232-241
Author(s):  
Yuan Wang ◽  
Man Zhao ◽  
Jinfeng Cui ◽  
Xin Wu ◽  
Yuehong Li ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Oxidative Phosphorylation ◽  
Ochratoxin A ◽  
Gastric Epithelium ◽  
Switching Energy

Metabolic signatures linked to macrophage polarization: from glucose metabolism to oxidative phosphorylation

2015 ◽  
Vol 43 (4) ◽  
pp. 740-744 ◽  
Author(s):  
Lisardo Boscá ◽  
Silvia González-Ramos ◽  
Patricia Prieto ◽  
María Fernández-Velasco ◽  
Marina Mojena ◽  
...  
Keyword(s):  
Immune Response ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Oxidative Phosphorylation ◽  
Metabolic Activity ◽  
Functional Role ◽  
Macrophage Activation ◽  
Macrophage Polarization ◽  
M1 Polarization ◽  
Different Types

Macrophages are present in a large variety of locations, playing distinct functions that are determined by its developmental origin and by the nature of the activators of the microenvironment. Macrophage activation can be classified as pro-inflammatory (M1 polarization) or anti-inflammatory-pro-resolution-deactivation (M2), these profiles coexisting in the course of the immune response and playing a relevant functional role in the onset of inflammation (Figure 1). Several groups have analysed the metabolic aspects associated with macrophage activation to answer the question about what changes in the regulation of energy metabolism and biosynthesis of anabolic precursors accompany the different types of polarization and to what extent they are necessary for the expression of the activation phenotypes. The interest of these studies is to regulate macrophage function by altering their metabolic activity in a ‘therapeutic way’.

Ochratoxin A induces G2 phase arrest in human gastric epithelium GES-1 cells in vitro

2010 ◽  
Vol 193 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Jinfeng Cui ◽  
Lingxiao Xing ◽  
Zengning Li ◽  
Sha Wu ◽  
Juan Wang ◽  
...  
Keyword(s):  
Ochratoxin A ◽  
Gastric Epithelium ◽  
Phase Arrest ◽  
G2 Phase

Retinal pH Reflects Retinal Energy Metabolism in the Day and Night

2004 ◽  
Vol 91 (6) ◽  
pp. 2404-2412 ◽  
Author(s):  
Andrey V. Dmitriev ◽  
Stuart C. Mangel
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Energy Production ◽  
Ph Gradient ◽  
Living Tissue ◽  
Selective Suppression ◽  
Subjective Night ◽  
Circadian Time ◽  
The Brain

The extracellular pH of living tissue in the retina and elsewhere in the brain is lower than the pH of the surrounding milieu. We have shown that the pH gradient between the in vitro retina and the superfusion solution is regulated by a circadian (24-h) clock so that it is smaller in the subjective day than in the subjective night. We show here that the circadian changes in retinal pH result from a clock-mediated change in the generation of H+ that accompanies energy production. To demonstrate this, we suppressed energy metabolism and recorded the resultant reduction in the pH difference between the retina and superfusate. The magnitude of the reduction in the pH gradient correlated with the extent of energy metabolism suppression. We also examined whether the circadian-induced increase in acid production during the subjective night results from an increase in energy metabolism or from the selective activation of glycolysis compared with oxidative phosphorylation. We found that the selective suppression of either oxidative phosphorylation or glycolysis had almost identical effects on the dynamics and extent of H+ production during the subjective day and night. Thus the proportion of glycolysis and oxidative phosphorylation is maintained the same regardless of circadian time, and the pH difference between the tissue and superfusion solution can therefore be used to evaluate total energy production. We conclude that circadian clock regulation of retinal pH reflects circadian regulation of retinal energy metabolism.

scholarly journals The Effects of Storage in vitro on Functions, Transcriptome, Proteome, and Oxidation Resistance of Giant Grouper Sperm

2021 ◽  
Vol 8 ◽  
Author(s):  
Yang Yang ◽  
Tong Wang ◽  
Sen Yang ◽  
Xi Wu ◽  
Wenhua Huang ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Oxidation Resistance ◽  
Cold Storage ◽  
Prolonged Storage ◽  
Negative Effects ◽  
Normal Functions ◽  
Oxidative Phosphorylation Pathway ◽  
The Absolute

Asynchrony of sexual maturity is a huge limitation in the reproduction of grouper sperm. Cold storage of sperm is an effective method to solve the problem of asynchronization. However, sperms gradually lose their activity with the prolonged storage time in vitro. In order to explore causes, the effects of cold storage on transcriptome, proteome and oxidation resistance of giant grouper sperm were analyzed. Firstly, the absolute RNA quantity and consistent transcripts existed in each spermatozoon were estimated. With the prolonged storage, the RNA quantity gradually decreased both in the cytoplasm and in the mitochondria of the spermatozoon. The decreased transcripts were mainly enriched with energy metabolism and stress response. Similar to RNAs, the absolute protein quantity was also significantly decreased during the storage of sperm. Decreased proteins were mainly enriched with the oxidative phosphorylation pathway. Proteins involved in the oxidative phosphorylation showed a faster degradation rate compared to the average total protein. In addition, the oxidation resistance and adenosine triphosphate (ATP) contents showed a significant decrease in the sperm during storage in vitro. These results implied that damages of transcriptome, proteome, and oxidation resistance have negative effects on the normal functions of sperm, especially their energy metabolism. The present study provides essential foundation for improving the storage of sperm in vitro.

scholarly journals Opposing effects of 2-deoxy-d-glucose on interictal- and ictal-like activity when K+ currents and GABAA receptors are blocked in rat hippocampus in vitro

2018 ◽  
Vol 119 (5) ◽  
pp. 1912-1923 ◽  
Author(s):  
Steen Nedergaard ◽  
Mogens Andreasen
Keyword(s):  
Glucose Metabolism ◽  
Oxidative Phosphorylation ◽  
Synaptic Transmission ◽  
Epileptiform Activity ◽  
Direct Consequence ◽  
In Vitro Models ◽  
Opposing Effects ◽  
Area Ca3 ◽  
Glucose Derivative

The ketogenic diet (KD), a high-fat, carbohydrate-restricted diet, is used as an alternative treatment for drug-resistant epileptic patients. Evidence suggests that compromised glucose metabolism has a significant role in the anticonvulsant action of the KD; however, it is unclear what part of the glucose metabolism that is important. The present study investigates how selective alterations in glycolysis and oxidative phosphorylation influence epileptiform activity induced by blocking K+ currents and GABAA and NMDA receptors in the hippocampal slice preparation. Blocking glycolysis with the glucose derivative 2-deoxy-d-glucose (2-DG; 10 mM) gave a fast reduction of the frequency of interictal discharge (IED) consistent with findings in other in vitro models. However, this was followed by the induction of seizure-like discharges in area CA1 and CA3. Substituting glucose with sucrose (glucopenia) had effects similar to those of 2-DG, whereas substitution with l-lactate or pyruvate reduced the IED but had a less proconvulsant effect. Blockade of ATP-sensitive K+ channels, glycine or adenosine 1 receptors, or depletion of the endogenous anticonvulsant compound glutathione did not prevent the actions of 2-DG. Baclofen (2 μM) reproduced the effect of 2-DG on IED activity. The proconvulsant effect of 2-DG could be reproduced by blocking the oxidative phosphorylation with the complex I toxin rotenone (4 μM). The data suggest that inhibition of IED, induced by 2-DG and glucopenia, is a direct consequence of impairment of glycolysis, likely exerted via a decreased recurrent excitatory synaptic transmission in area CA3. The accompanying proconvulsant effect is caused by an excitatory mechanism, depending on impairment of oxidative phosphorylation. NEW & NOTEWORTHY This study reveals two opposing effects of 2-deoxy-d-glucose (2-DG) and glucopenia on in vitro epileptiform discharge observed during combined blockade of K+ currents and GABAA receptors. Interictal-like activity is inhibited by a mechanism that selectively depends on impairment of glycolysis and that results from a decrease in the strength of excitatory recurrent synaptic transmission in area CA3. In contrast, 2-DG and glucopenia facilitate ictal-like activity by an excitatory mechanism, depending on impairment of mitochondrial oxidative phosphorylation.

Melatonin modifies tumor hypoxia and metabolism by inhibiting HIF-1α and energy metabolic pathway in the in vitro and in vivo models of breast cancer

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Carbonic Anhydrases ◽  
In Vivo Models ◽  
Ca Ix ◽  
Gene And Protein Expression

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 

In Vitro Diabetogenic Effect of Cadmium on Liver

2017 ◽  
Vol 8 (01) ◽  
Author(s):  
Agung Biworo ◽  
Dwi Rezki Amalia ◽  
Gratianus Billy Himawan ◽  
Lisda Rizky Amalia ◽  
Valentina Halim ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Liver Homogenate ◽  
Liver Cells ◽  
Male Rats ◽  
Glycogen Level ◽  
Liver Sample ◽  
Km Value ◽  
Cd Exposure ◽  
Menten Constant

The objectives of this study were to determine the effect of cadmium (Cd) on glucose metabolism disruption in liver cells homogenate in vitro. The glucose metabolism disruption was analyzed by measuring the level of liver glucose, glycogen and methylglyoxal (MG), and the activity of glucokinase activity. In this experiment, a liver sample was taken from male rats (Rattus novergicus). Samples then homogenized and divided into four groups with; C served as control which contains liver homogenate only; T1 which contains liver homogenate + 0.03 mg/l of cadmium sulphate (CdSO4); T2 which contains liver homogenate + 0.3 mg/l of CdSO4; and T3 which contains liver homogenate + 3 mg/l of CdSO4. After treatment, liver glucose, glycogen, and MG levels, and glucokinase activity were estimated. The activity of liver glucokinase was estimated by measuring the Michaelis-Menten constant (Km) value. The results revealed that Cd exposure could significantly increase glucose and MG levels, the Km value of glucokinase, and decreased the glycogen level in liver cells (P>0.05). These results indicated that Cd exposure induced the disruption of glucose metabolism in the liver.

scholarly journals Nutrient Deficiency Promotes the Entry of Helicobacter pylori Cells into Candida Yeast Cells

Biology ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 426
Author(s):  
Kimberly Sánchez-Alonzo ◽  
Fabiola Silva-Mieres ◽  
Luciano Arellano-Arriagada ◽  
Cristian Parra-Sepúlveda ◽  
Humberto Bernasconi ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Nutrient Deficiency ◽  
Gastric Epithelium ◽  
Yeast Cells ◽  
Nutrient Concentrations ◽  
Fetal Bovine ◽  
H Pylori ◽  
Pcr Techniques ◽  
Strain Dependent

Helicobacter pylori, a Gram-negative bacterium, has as a natural niche the human gastric epithelium. This pathogen has been reported to enter into Candida yeast cells; however, factors triggering this endosymbiotic relationship remain unknown. The aim of this work was to evaluate in vitro if variations in nutrient concentration in the cultured medium trigger the internalization of H. pylori within Candida cells. We used H. pylori–Candida co-cultures in Brucella broth supplemented with 1%, 5% or 20% fetal bovine serum or in saline solution. Intra-yeast bacteria-like bodies (BLBs) were observed using optical microscopy, while intra-yeast BLBs were identified as H. pylori using FISH and PCR techniques. Intra-yeast H. pylori (BLBs) viability was confirmed using the LIVE/DEAD BacLight Bacterial Viability kit. Intra-yeast H. pylori was present in all combinations of bacteria–yeast strains co-cultured. However, the percentages of yeast cells harboring bacteria (Y-BLBs) varied according to nutrient concentrations and also were strain-dependent. In conclusion, reduced nutrients stresses H. pylori, promoting its entry into Candida cells. The starvation of both H. pylori and Candida strains reduced the percentages of Y-BLBs, suggesting that starving yeast cells may be less capable of harboring stressed H. pylori cells. Moreover, the endosymbiotic relationship between H. pylori and Candida is dependent on the strains co-cultured.

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