oxidative metabolism
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2022 ◽  
Vol 146 ◽  
pp. 1-11
Cristine Bonacina ◽  
Rayane Monique Sete da Cruz ◽  
Andressa Bezerra Nascimento ◽  
Letícia Neris Barbosa ◽  
José Eduardo Gonçalves ◽  

Xenobiotica ◽  
2022 ◽  
pp. 1-13
Ayaka Kojima ◽  
Ayuka Sogabe ◽  
Masayuki Nadai ◽  
Miki Katoh

2022 ◽  
Vol 145 ◽  
pp. 112391
Katarína Vavrová ◽  
Radek Indra ◽  
Petr Pompach ◽  
Zbyněk Heger ◽  
Petr Hodek

Cell Reports ◽  
2022 ◽  
Vol 38 (1) ◽  
pp. 110197
Adrien Grenier ◽  
Laury Poulain ◽  
Johanna Mondesir ◽  
Arnaud Jacquel ◽  
Claudie Bosc ◽  

Jane Stremming ◽  
Eileen Chang ◽  
Leslie A Knaub ◽  
Michael L Armstrong ◽  
Peter R Baker ◽  

Skeletal muscle from the late gestation sheep fetus with intrauterine growth restriction (IUGR) has evidence of reduced oxidative metabolism. Using a sheep model of placental insufficiency and IUGR, we tested the hypothesis that by late gestation, IUGR fetal skeletal muscle has reduced capacity for oxidative phosphorylation due to intrinsic deficits in mitochondrial respiration. We measured mitochondrial respiration in permeabilized muscle fibers from biceps femoris (BF) and soleus (SOL) from control and IUGR fetal sheep. Using muscles including BF, SOL, tibialis anterior (TA), and flexor digitorum superficialis (FDS), we measured citrate synthase (CS) activity, mitochondrial complex subunit abundance, fiber type distribution, and gene expression of regulators of mitochondrial biosynthesis. Ex vivo mitochondrial respiration was similar in control and IUGR muscle. However, CS activity was lower in IUGR BF and TA, indicating lower mitochondrial content, and protein expression of individual mitochondrial complex subunits was lower in IUGR TA and BF in a muscle specific pattern. IUGR TA, BF, and FDS also had lower expression of type I oxidative fibers. Fiber type shifts that support glycolytic instead of oxidative metabolism may be advantageous for the IUGR fetus in a hypoxic and nutrient deficient environment, whereas these adaptions may be maladaptive in postnatal life.

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Yi Gan ◽  
Xiufeng Chen ◽  
Ruokun Yi ◽  
Xin Zhao

Lactobacillus plantarum ZS62 is a newly isolated strain from naturally fermented yogurt that might offer some beneficial effects in the setting of alcohol-induced subacute liver injury. The liver-protective effect of L. plantarum ZS62 was investigated by gavage feeding of mice with this Lactobacillus strain ( 1 × 10 9 CFU/kg BW) before alcohol administration daily for 7 days. We then compared hepatic morphology, liver function indexes, liver lipid levels, inflammation, oxidative stress levels, and mRNA expression of oxidative metabolism- and inflammation-related genes in mice that had been pretreated with Lactobacillus plantarum versus control mice that had not been pretreated. Our results showed that L. plantarum ZS62 attenuated alcohol-induced weight loss; prevented morphological changes in hepatocytes; reduced markers of liver damage including aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), hyaluronidase (HAase), precollagen III (PC III), and inflammatory cytokines; and enhanced the antioxidative status. L. plantarum ZS62 also significantly downregulated inflammation-related genes and upregulated lipid- and oxidative-metabolism genes. Thus, Lactobacillus plantarum pretreatment appears to confer hepatic protection by reducing inflammation and enhancing antioxidative capacity. The protective effect of L. plantarum ZS62 was even better than that of a commonly used commercial lactic acid bacteria (Lactobacillus delbrueckii subsp. Bulgaricus). The L. plantarum ZS62 might be a potentially beneficial prophylactic treatment for people who frequently drink alcoholic beverages.

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 901-901
Brian Andonian ◽  
David Bartlett ◽  
Nancie MacIver ◽  
William Kraus ◽  
Kim Huffman

Abstract Persons with rheumatoid arthritis (RA) have poor cardiorespiratory fitness and accelerated biological aging driven by systemic impairments in metabolism and inflammation. In this study of older RA participants, our goal was to identify the effects of a high-intensity interval training (HIIT) program on cardiorespiratory fitness and peripheral CD4+ T cell metabolism. We isolated CD4+ T cells from peripheral blood mononuclear cells in sedentary female RA participants (n=6; age=64.0+/-6.3 years) who underwent cardiopulmonary exercise testing and phlebotomy before and after 10 weeks of HIIT. HIIT improved RA cardiorespiratory fitness by 6.5+/-6.0% (pre-HIIT VO2 peak=25.1+/-5.1 ml/kg/min, post-HIIT VO2 peak=26.7+/-5.0; p=0.05). As measured by Seahorse XF Mito Stress Test, there were no significant mean changes in CD4+ T cell oxidative (oxygen consumption rate (OCR); pmol/min) or glycolytic (extracellular acidification rate (ECAR); mpH/min) metabolism, however there was large interindividual variability. RA peripheral CD4+ T cells preferred glycolytic metabolism (pre-HIIT mean basal OCR/ECAR ratio=0.78+/-0.13 pmol/mpH), while HIIT non-significantly shifted cellular preference toward oxidative metabolism (post-HIIT mean basal OCR/ECAR ratio=0.86+/-0.16; p=0.30). Increases in RA cardiorespiratory fitness following HIIT were significantly associated with increases in RA peripheral CD4+ T cell OCR/ECAR ratio (Spearman’s rho=1.0, p<0.001) and basal and maximal respiration (rho=0.89, p=0.02 for both). Additionally, increases in CD4+ T cell mitochondrial ATP-linked respiration were significantly associated with increased quantities of circulating naïve CD4+CCR7+CD45RA+ T cells (rho=0.89, p=0.02). Our findings suggest that targeting cardiorespiratory fitness may be key in modulating T cell specific oxidative metabolism and function to prevent immunosenescence in older patients with chronic inflammatory diseases.

2021 ◽  
Bohye Park ◽  
Ji Yeon Kim ◽  
Olivia F. Riffey ◽  
Antje Bruckbauer ◽  
James McLoughlin ◽  

Abstract Colorectal cancer (CRC) cells shift metabolism toward aerobic glycolysis and away from using oxidative substrates such as butyrate. Pyruvate kinase M1/2 (PKM) is an enzyme that catalyzes the last step in glycolysis, which converts phosphoenolpyruvate to pyruvate. M1 and M2 are alternatively spliced isoforms of the Pkm gene. The PKM1 isoform promotes oxidative metabolism, whereas PKM2 enhances aerobic glycolysis. We hypothesize that the PKM isoforms are involved in the shift away from butyrate oxidation towards glycolysis in CRC cells. Here, we find that PKM2 is increased and PKM1 is decreased in human colorectal carcinomas as compared to non-cancerous tissue. To test whether PKM1/2 alter colonocyte metabolism, we created a knockdown of PKM2 and PKM1 in CRC cells to analyze how butyrate oxidation and glycolysis would be impacted. We report that butyrate oxidation in CRC cells is regulated by PKM1 levels, not PKM2. Decreased butyrate oxidation observed through knockdown of PKM1 and PKM2 is rescued through re-addition of PKM1. Diminished PKM1 lowered mitochondrial basal respiration and decreased mitochondrial spare capacity. We demonstrate that PKM1 suppresses glycolysis and inhibits hypoxia-inducible factor-1 alpha. These data suggest that reduced PKM1 is, in part, responsible for increased glycolysis and diminished butyrate oxidation in CRC cells.

2021 ◽  
Vol 41 ◽  
pp. 100419
Shotaro Uehara ◽  
Nao Yoneda ◽  
Yuichiro Higuchi ◽  
Hiroshi Yamazaki ◽  
Hiroshi Suemizu

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