• Title/Summary/Keyword: cell metabolism

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Search for acetaldehyde trapping agents by using alcohol dehydrogenase assay

  • Lee, Hyun-Joo;Lee, Kang-Man
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.160.3-161
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    • 2003
  • Aldehyde and active form of free oxygen produced in alcohol metabolism in liver are the cause of liver cell damage. The main system of alcohol metabolism is composed of alcohol dehydrogenase(ADH), aldehyde dehydrogenase(ALDH) and cytochrome P4502E1. Alcohol dehydrogenase is reversible in alcohol metabolism. To block the backward reaction and enhance alcohol oxidation, acetaldehyde trapping agents were assayed. The assay was carried out by measuring decreasing NADH at 340nm, using acetaldcehyde and NADH as substrate and coenzyme respectively. (omitted)

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Regulation of mitochondrial morphology and metabolism by Jak-STAT pathway

  • Rhee, Kun Do
    • Journal of Animal Reproduction and Biotechnology
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    • v.36 no.4
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    • pp.189-193
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    • 2021
  • Jak-STAT pathway is required for embryogenesis, female gametogenesis, cytokine-mediated neuroprotection, diabetes, obesity, cancer, stem cell, and various tissues. The noncanonical role of Jak-STAT in mitochondria function was supported by the detection of STAT protein in mitochondria, however, several studies show that STAT protein is detected in the endoplasmic reticulum (ER), and not in mitochondria. STAT protein may alter mitochondria function without entering mitochondria, this involves regulation of fission and fusion proteins to change mitochondria morphology. However, how changes in mitochondria morphology lead to changes in mitochondria metabolism needs further investigation.

Anticancer Effects of Gut Microbiota-Derived Short-Chain Fatty Acids in Cancers

  • Mi-Young Son;Hyun-Soo Cho
    • Journal of Microbiology and Biotechnology
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    • v.33 no.7
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    • pp.849-856
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    • 2023
  • Short-chain fatty acids (SCFAs), such as butyrate, propionate, and acetate produced by the gut microbiota have been implicated in physiological responses (defense mechanisms, immune responses, and cell metabolism) in the human body. In several types of cancers, SCFAs, especially butyrate, suppress tumor growth and cancer cell metastasis via the regulation of the cell cycle, autophagy, cancer-related signaling pathways, and cancer cell metabolism. In addition, combination treatment with SCFAs and anticancer drugs exhibits synergistic effects, increasing anticancer treatment efficiency and attenuating anticancer drug resistance. Therefore, in this review, we point out the importance of SCFAs and the mechanisms underlying their effects in cancer treatment and suggest using SCFA-producing microbes and SCFAs to increase therapeutic efficacy in several types of cancers.

Metabolic Challenges in Anticancer CD8 T Cell Functions

  • Andrea M. Amitrano;Minsoo Kim
    • IMMUNE NETWORK
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    • v.23 no.1
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    • pp.9.1-9.15
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    • 2023
  • Cancer immunotherapies continue to face numerous obstacles in the successful treatment of solid malignancies. While immunotherapy has emerged as an extremely effective treatment option for hematologic malignancies, it is largely ineffective against solid tumors due in part to metabolic challenges present in the tumor microenvironment (TME). Tumor-infiltrating CD8+ T cells face fierce competition with cancer cells for limited nutrients. The strong metabolic suppression in the TME often leads to impaired T-cell recruitment to the tumor site and hyporesponsive effector functions via T-cell exhaustion. Growing evidence suggests that mitochondria play a key role in CD8+ T-cell activation, migration, effector functions, and persistence in tumors. Therefore, targeting the mitochondrial metabolism of adoptively transferred T cells has the potential to greatly improve the effectiveness of cancer immunotherapies in treating solid malignancies.

Exploring differentially expressed genes related to metabolism by RNA-Seq in porcine embryonic fibroblast after insulin treatment

  • Yingjuan, Liang;Jinpeng, Wang;Xinyu, Li;Shuang, Wu;Chaoqian, Jiang;Yue, Wang;Xuechun, Li;Zhong-Hua, Liu;Yanshuang, Mu
    • Journal of Veterinary Science
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    • v.23 no.6
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    • pp.90.01-90.13
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    • 2022
  • Background: Insulin regulates glucose homeostasis and has important effects on metabolism, cell growth, and differentiation. Depending on the cell type and physiological context, insulin signal has specific pathways and biological outcomes in different tissues and cells. For studying the signal pathway of insulin on glycolipid metabolism in porcine embryonic fibroblast (PEF), we used high-throughput sequencing to monitor gene expression patterns regulated by insulin. Objectives: The goal of our research was to see how insulin affected glucose and lipid metabolism in PEFs. Methods: We cultured the PEFs with the addition of insulin and sampled them at 0, 48, and 72 h for RNA-Seq analysis in triplicate for each time point. Results: At 48 and 72 h, 801 and 1,176 genes were differentially expressed, respectively. Of these, 272 up-regulated genes and 264 down-regulated genes were common to both time points. Gene Ontology analysis was used to annotate the functions of the differentially expressed genes (DEGs), the biological processes related to lipid metabolism and cell cycle were dominant. And the DEGs were significantly enriched in interleukin-17 signaling pathway, phosphatidylinositol-3-kinase-protein kinase B signaling pathway, pyruvate metabolism, and others pathways related to lipid metabolism by Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Conclusions: These results elucidate the transcriptomic response to insulin in PEF. The genes and pathways involved in the transcriptome mechanisms provide useful information for further research into the complicated molecular processes of insulin in PEF.

Cancer Energy Metabolism: Shutting Power off Cancer Factory

  • Kim, Soo-Youl
    • Biomolecules & Therapeutics
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    • v.26 no.1
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    • pp.39-44
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    • 2018
  • In 1923, Dr. Warburg had observed that tumors acidified the Ringer solution when 13 mM glucose was added, which was identified as being due to lactate. When glucose is the only source of nutrient, it can serve for both biosynthesis and energy production. However, a series of studies revealed that the cancer cell consumes glucose for biosynthesis through fermentation, not for energy supply, under physiological conditions. Recently, a new observation was made that there is a metabolic symbiosis in which glycolytic and oxidative tumor cells mutually regulate their energy metabolism. Hypoxic cancer cells use glucose for glycolytic metabolism and release lactate which is used by oxygenated cancer cells. This study challenged the Warburg effect, because Warburg claimed that fermentation by irreversible damaging of mitochondria is a fundamental cause of cancer. However, recent studies revealed that mitochondria in cancer cell show active function of oxidative phosphorylation although TCA cycle is stalled. It was also shown that blocking cytosolic NADH production by aldehyde dehydrogenase inhibition, combined with oxidative phosphorylation inhibition, resulted in up to 80% decrease of ATP production, which resulted in a significant regression of tumor growth in the NSCLC model. This suggests a new theory that NADH production in the cytosol plays a key role of ATP production through the mitochondrial electron transport chain in cancer cells, while NADH production is mostly occupied inside mitochondria in normal cells.

Cancer Metabolism: Strategic Diversion from Targeting Cancer Drivers to Targeting Cancer Suppliers

  • Kim, Soo-Youl
    • Biomolecules & Therapeutics
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    • v.23 no.2
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    • pp.99-109
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    • 2015
  • Drug development groups are close to discovering another pot of gold-a therapeutic target-similar to the success of imatinib (Gleevec) in the field of cancer biology. Modern molecular biology has improved cancer therapy through the identification of more pharmaceutically viable targets, and yet major problems and risks associated with late-phase cancer therapy remain. Presently, a growing number of reports have initiated a discussion about the benefits of metabolic regulation in cancers. The Warburg effect, a great discovery approximately 70 years ago, addresses the "universality" of cancer characteristics. For instance, most cancer cells prefer aerobic glycolysis instead of mitochondrial respiration. Recently, cancer metabolism has been explained not only by metabolites but also through modern molecular and chemical biological techniques. Scientists are seeking context-dependent universality among cancer types according to metabolic and enzymatic pathway signatures. This review presents current cancer metabolism studies and discusses future directions in cancer therapy targeting bio-energetics, bio-anabolism, and autophagy, emphasizing the important contribution of cancer metabolism in cancer therapy.

Mass spectrometry-based approaches to explore metabolism regulating ferroptosis

  • Nguyen, Chi Thi Ngoc;Kim, Seon Min;Kang, Yun Pyo
    • BMB Reports
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    • v.55 no.9
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    • pp.413-416
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    • 2022
  • Ferroptosis is a type of programmed cell death distinct from apoptosis or necroptosis. Ferroptosis is well characterized by an iron-dependent accumulation of lipid peroxides and disruption of cellular membrane integrity. Many metabolic alterations can prevent or accelerate ferroptosis induction. Recent advances in analytical techniques of mass spectrometry have allowed high-throughput analysis of metabolites known to be critical for understanding ferroptosis regulatory metabolism. In this review, we introduce mass spectrometry-based analytical methods contributing to recent discovery of various metabolic pathways regulating ferroptosis, focusing on cysteine metabolism, antioxidant metabolism, and poly-unsaturated fatty acid metabolism.

Effects of Palmijihwangtang (PMT) and Exercise on Glucose Metabolism in Myocardium Cell Membrane and Pancreas $\beta$-Cell of Zucker Diabetic Fatty Rats

  • Lee Myeong-Jong
    • The Journal of Korean Medicine
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    • v.25 no.4
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    • pp.200-208
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    • 2004
  • Objective: Non-insulin Dependent Diabetes Mellitus (NIDDM) is characterized by insulin resistance, which affects the glucose transportation inside the cell. The purpose of this study was to find out how Palmijihwangtang (PMT) and exercise influence the glucose transport metabolism in the organ muscles of ZDF (zucker diabetic fatty) rat with insulin resistance. Methods: Using three male normal zucker rats and twelve male obese rats, they were divided into a normal lean group (N=3), obese control group (N=3), obese exercises group (N=3), obese medication group (N=3), obese exercise and medication group (N=3). Treadmill exercise were repeated with 27m/min speed for an hour a day, five days a week, for 8 weeks. And 20β/sub ¢/ of PMT was orally administered twice a day for 8 weeks, after that a period blood sample was exsanguinated by heart perforation and was analyzed. Results: The body weight of the OM and OEM group showed a significant decrease among all the obese groups. The blood insulin level increased significantly of all groups in comparison with the N group. All of the OE, OM and the OEM groups showed a significant decrease of insulin level compared with the OC group; especially the OEM group demonstrated the most among obese groups. Regarding GLUT-4 level, OEM was the unique group showed a significant increase among all the obese groups. The VAMP-2 level in myocardium cell membrane was increased significantly at OC group in comparison with the N group, whereas the OEM group only showed significant decrease of it. In addition, the VAMP-2 level in pancreas β-cell was significantly decreased at all the obese groups in comparison with the N group. Only the OEM group showed significant increase among all the obese groups. Conclusion: Palmijihwangtang (PMT) and exercise could effectively promote the insulin metabolism in pancreas β-cells and activate the glucose transport process in myocardium cell membrane by lowering the insulin resistance of ZDF rats.

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