scholarly journals Effects of Moxibustion and Moxa Smoke on Behavior Changes and Energy Metabolism in APP/PS1 Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Lue Ha ◽  
Mengyun Yu ◽  
Zhiyi Yan ◽  
Zhang Rui ◽  
Baixiao Zhao
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Negative Control ◽  
Control Group ◽  
Behavioral Tests ◽  
Acid Cycle ◽  
Moxibustion Group ◽  
Model Control

Objective. To investigate the antiaging effects of moxibustion and moxa smoke on APP/PS1 mice and to illustrate the mechanism of moxibustion improving Alzheimer’s disease (AD). Methods. 36 male APP/PS1 mice were randomly assigned into three groups (n = 12), including a model control group, a moxibustion group, and a moxa smoke group. In addition, 12 C57BL/6 normal mice served as a normal (negative) control group. Mice in the moxibustion group received moxibustion intervention using Guanyuan (RN4) acupoint. Mice in the moxa smoke group received moxa smoke exposure with the same frequency as the moxibustion group. Behavioral tests were implemented in the 9th week, 3 days after the completion of the intervention. Tricarboxylic acid cycle and fatty acid metabolomics assessments of the mice were determined after behavioral tests. Results. In this study, relative to normal mice, we found that AD mice showed altered tricarboxylic and fatty acid metabolism and showed behavioral changes consistent with the onset of AD. However, both the moxibustion and moxa smoke interventions were able to mitigate these effects to some degree in AD mice. Conclusions. The data suggest that tricarboxylic acid cycle and unsaturated fatty acid metabolomics changes may be a target of AD, and the beneficial effects of moxibustion on cognitive behaviors may be mediated by the energy metabolism system.

scholarly journals Detection of myocardial medium‐chain fatty acid oxidation and tricarboxylic acid cycle activity with hyperpolarized [1– 13 C]octanoate

2020 ◽  
Vol 33 (3) ◽  
Author(s):  
Hikari A.I. Yoshihara ◽  
Jessica A.M. Bastiaansen ◽  
Magnus Karlsson ◽  
Mathilde H. Lerche ◽  
Arnaud Comment ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Chain Fatty Acid ◽  
Medium Chain Fatty Acid ◽  
Acid Oxidation ◽  
Acid Cycle ◽  
Medium Chain

scholarly journals Role of Energy Metabolism in the Progression of Neuroblastoma

2021 ◽  
Vol 22 (21) ◽  
pp. 11421
Author(s):  
Monika Sakowicz-Burkiewicz ◽  
Tadeusz Pawełczyk ◽  
Marlena Zyśk
Keyword(s):  
Energy Metabolism ◽  
Extracellular Vesicles ◽  
Tricarboxylic Acid Cycle ◽  
Significant Risk ◽  
Metabolic Enzymes ◽  
Genetic Alterations ◽  
Tricarboxylic Acid ◽  
Primary Role ◽  
Acid Cycle ◽  
Risk Of Death

Neuroblastoma is a common childhood cancer possessing a significant risk of death. This solid tumor manifests variable clinical behaviors ranging from spontaneous regression to widespread metastatic disease. The lack of promising treatments calls for new research approaches which can enhance the understanding of the molecular background of neuroblastoma. The high proliferation of malignant neuroblastoma cells requires efficient energy metabolism. Thus, we focus our attention on energy pathways and their role in neuroblastoma tumorigenesis. Recent studies suggest that neuroblastoma-driven extracellular vesicles stimulate tumorigenesis inside the recipient cells. Furthermore, proteomic studies have demonstrated extracellular vesicles (EVs) to cargo metabolic enzymes needed to build up a fully operative energy metabolism network. The majority of EV-derived enzymes comes from glycolysis, while other metabolic enzymes have a fatty acid β-oxidation and tricarboxylic acid cycle origin. The previously mentioned glycolysis has been shown to play a primary role in neuroblastoma energy metabolism. Therefore, another way to modify the energy metabolism in neuroblastoma is linked with genetic alterations resulting in the decreased activity of some tricarboxylic acid cycle enzymes and enhanced glycolysis. This metabolic shift enables malignant cells to cope with increasing metabolic stress, nutrition breakdown and an upregulated proliferation ratio.

scholarly journals Metabolic changes in the lymphocytes during influenza

2012 ◽  
Vol 93 (4) ◽  
pp. 580-584
Author(s):  
I V Sergeeva ◽  
N I Kamzalakova ◽  
E P Tikhonova ◽  
G V Bulygin
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Tricarboxylic Acid Cycle ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Tricarboxylic Acid ◽  
Nicotinamide Adenine ◽  
Control Group ◽  
Healthy Individuals ◽  
Acid Cycle ◽  
Intracellular Enzymes ◽  
Glucose 6 Phosphate Dehydrogenase

Aim. To assess the nature and intensity of metabolic processes in lymphocytes of patients with influenza according to the activity of intracellular enzymes in comparison to the severity of the disease. Methods. Determined were the enzymatic parameters of lymphocytes of 45 patients aged 18 to 42 years with a diagnosis of «influenza». Two groups of patients were formed: with moderate (24 patients) and severe (21 patients) course of the disease. Used as controls were the values the activity of intracellular enzymes of lymphocytes of 37 practically healthy individuals of comparable age. Results. In patients with a moderately severe course of the influenza compared with the controls noted was a significant increase in activity of glucose-6-phosphate dehydrogenase (3.17±0.53 and 2.74±0.31 mkE/10 000 cells, p 0.05) and glycerol-3-phosphate dehydrogenase (57.33±±5.65 and 0.84±0.16 mkE/10 000 cells respectively, p 0.001). The activity of lactate dehydrogenase was lower in patients than in controls (0.40±0.08 and 0.84±0.08 mkE/10 000 cells respectively, p 0.001). Indicators of nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate dependant isocitrate dehydrogenases in lymphocytes of patients were lower than in the controls: the first indicator in the patients was 0.17±0.02 mkE/10 000 cells, in controls - 1.95±0.25 mkE/10 000 cells (p 0.001), and for the second indicator these values were respectively 0.09±0.01 and 31.02±±2.20 mkE/10 000 cells (p 0.001). In patients with a moderately severe course of influenza the activity of nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate dependant glutamate dehydrogenases was significantly higher compared with healthy individuals: 63.67±5.32 and 0.34±0.06 mkE/10 000 cells, 1.45±0.18 and 0.11±0.02 mkE/10 000 cells respectively (p 0.001). The activity of nicotinamide adenine dinucleotide dependant malate dehydrogenase in patients was equal to 86.46±12.30 mkE/10 000 cells (in the control group 84.16±13.70 mkE/10 000 cells), and the activity of nicotinamide adenine dinucleotide phosphate dependant malate dehydrogenase was equal to 1.34±±0.25 mkE/10 000 cells (in the control group 0.33±0.07 mkE/10 000 cells, p 0.001). The activity of glutathione reductase was also higher in patients with the moderately severe course of the influenza: 5.86±0.25 mkE/10 000 cells, while the value in healthy individuals was 1.28±0.30 mkE/10 000 cells (p 0.001). In the group of patients with a severe course of influenza the activity of almost all (except for glucose-6-phosphate dehydrogenase) enzymes was higher than during the moderately severe course of disease. Conclusion. At the peak of the diseases noted were opposite changes in the activity of reactions of the pentose phosphate cycle and glycolysis. With a high functional load on the cells there is a significant reduction in the intensity of the reactions of the initial phase of the tricarboxylic acid cycle, which reduces the energy efficiency of the cycle, while the intense influx of metabolites to supply the tricarboxylic acid cycle with substrates of the amino acid metabolism provides enhanced transport of amino acids into the lymphocytes.

Characterization of urinary biomarkers and their relevant mechanisms of zoledronate-induced nephrotoxicity using rats and HK-2 cells

2019 ◽  
Vol 38 (5) ◽  
pp. 598-609
Author(s):  
Z Lan ◽  
K Chai ◽  
Y Jiang ◽  
X Liu
Keyword(s):  
Oxidative Stress ◽  
Tricarboxylic Acid Cycle ◽  
Kidney Injury ◽  
Urinary Metabolites ◽  
Tricarboxylic Acid ◽  
Glutathione Metabolism ◽  
Control Group ◽  
Acid Cycle ◽  
Urinary Levels ◽  
Group 3

The aim of this study was to identify biomarkers of zoledronate-induced nephrotoxicity and to further characterize the mechanisms underlying this process by analyzing urinary metabolites. Twenty-four rats were randomly divided into four groups containing four (two control groups) or eight rats (two zoledronate groups) per group. The rats were injected intravenously with saline or zoledronate (3 mg/kg) singly (single, 3 weeks) or repeatedly eight times (3 weeks/time, 24 weeks). Serum blood urea nitrogen, serum creatinine, creatinine clearance, and kidney injury observed by hematoxylin and eosin and immunohistochemical staining were changed only in the repeated zoledronate group (3 mg/kg, 3 weeks/time, 24 weeks). Urinary levels of S-adenosylmethionine, S-adenosylhomocysteine, l-cystathionine, l-γ-glutamylcysteine, and glutathione related to glutathione metabolism and fumaric acid and succinic acid related to the tricarboxylic acid cycle in the zoledronate-treated group (3 mg/kg, 3 weeks/time, 24 weeks) were significantly lower than those in the control group, suggesting that zoledronate may cause cellular oxidative stress. Besides, urinary levels of uracil and uridine related to pyrimidine metabolism also decreased after zoledronate treatment (3 mg/kg, 3 weeks/time, 24 weeks), while the levels of hypoxanthine related to purine metabolism, histamine related to histamine metabolism, and several amino acids were significantly increased. Moreover, zoledronate-induced enhanced oxidative stress and histamine overproduction were confirmed by reactive oxygen species (ROS) and histamine measurement in a human proximal tubular cell line. Taken together, zoledronate-induced nephrotoxicity may be attributed to it inducing perturbations in glutathione biosynthesis and the tricarboxylic acid cycle, further causing ROS overproduction, oxidative stress, and cellular inflammation, thereby leading to nephrotoxicity.

Effect of Ca2+ on cardiac mitochondrial energy production is modulated by Na+ and H+ dynamics

2007 ◽  
Vol 292 (6) ◽  
pp. C2004-C2020 ◽  
Author(s):  
My-Hanh T. Nguyen ◽  
S. J. Dudycha ◽  
M. Saleet Jafri
Keyword(s):  
Energy Metabolism ◽  
Energy Production ◽  
Hydrogen Exchange ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Calcium Dynamics ◽  
Mitochondrial Energy Metabolism ◽  
Acid Cycle ◽  
Atp Production ◽  
Sodium Hydrogen

The energy production of mitochondria in heart increases during exercise. Several works have suggested that calcium acts at multiple control points to activate net ATP production in what is termed “parallel activation”. To study this, a computational model of mitochondrial energy metabolism in the heart has been developed that integrates the Dudycha-Jafri model for the tricarboxylic acid cycle with the Magnus-Keizer model for mitochondrial energy metabolism and calcium dynamics. The model improves upon the previous formulation by including an updated formulation for calcium dynamics, and new descriptions of sodium, hydrogen, phosphate, and ATP balance. To this end, it incorporates new formulations for the calcium uniporter, sodium-calcium exchange, sodium-hydrogen exchange, the F1F0-ATPase, and potassium-hydrogen exchange. The model simulates a wide range of experimental data, including steady-state and simulated pacing protocols. The model suggests that calcium is a potent activator of net ATP production and that as pacing increases energy production due to calcium goes up almost linearly. Furthermore, it suggests that during an extramitochondrial calcium transient, calcium entry and extrusion cause a transient depolarization that serve to increase NADH production by the tricarboxylic acid cycle and NADH consumption by the respiration driven proton pumps. The model suggests that activation of the F1F0-ATPase by calcium is essential to increase ATP production. In mitochondria very close to the release sites, the depolarization is more severe causing a temporary loss of ATP production. However, due to the short duration of the depolarization the net ATP production is also increased.

scholarly journals Bioenergetic Analysis of Single Pancreatic β-Cells Indicates an Impaired Metabolic Signature in Type 2 Diabetic Subjects

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3496-3503 ◽  
Author(s):  
Akos A. Gerencser
Keyword(s):  
Insulin Secretion ◽  
Membrane Potential ◽  
Energy Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Atp Synthesis ◽  
Tricarboxylic Acid ◽  
Β Cells ◽  
Acid Cycle ◽  
Type 2 Diabetic

Impaired activation of mitochondrial energy metabolism by glucose has been demonstrated in type 2 diabetic β-cells. The cause of this dysfunction is unknown. The aim of this study was to identify segments of energy metabolism with normal or with altered function in human type 2 diabetes mellitus. The mitochondrial membrane potential (ΔψM), and its response to glucose, is the main driver of mitochondrial ATP synthesis and is hence a central mediator of glucose-induced insulin secretion, but its quantitative determination in β-cells from human donors has not been attempted, due to limitations in assay technology. Here, novel fluorescence microscopic assays are exploited to quantify ΔψM and its response to glucose and other secretagogues in β-cells of dispersed pancreatic islet cells from 4 normal and 3 type 2 diabetic organ donors. Mitochondrial volume densities and the magnitude of ΔψM in low glucose were not consistently altered in diabetic β-cells. However, ΔψM was consistently less responsive to elevation of glucose concentration, whereas the decreased response was not observed with metabolizable secretagogue mixtures that feed directly into the tricarboxylic acid cycle. Single-cell analysis of the heterogeneous responses to metabolizable secretagogues indicated no dysfunction in relaying ΔψM hyperpolarization to plasma membrane potential depolarization in diabetic β-cells. ΔψM of diabetic β-cells was distinctly responsive to acute inhibition of ATP synthesis during glucose stimulation. It is concluded that the mechanistic deficit in glucose-induced insulin secretion and mitochondrial hyperpolarization of diabetic human β-cells is located upstream of the tricarboxylic acid cycle and manifests in dampening the control of ΔψM by glucose metabolism.

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