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Impact of Probiotics on Human Gut Microbiota and the Relationship with Obesity
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Fernanda Bianchi, Katia Sivieri
It has been suggested that the modulation of the expression of genes involved in inflammation and fatty acid oxidation, such as tumour necrosis factor alpha (TNFα), Interleukin 6 (IL6), PPARγ coactivator-1 alpha (PGC1α), IL1B, chemokine ligand 2 (CCL2), Carnitine palmitoyltransferase I and II (CPT1 and CPT2), and Acyl-CoA Oxidase 1 (ACOX1), are the most frequently-involved mechanisms in the probiotic’s anti-obesity effects. The exact genes modulated are dependent on the strain (Park et al. 2013, Miyoshi et al. 2014).
Mitochondrial Dysfunction and Oxidative Stress in the Pathogenesis of Metabolic Syndrome
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
FA derivatives from lipolysis, lipogenesis or FA catabolism are ligands of PPARa. Free fatty acids, including long-chain polyunsaturated FAs (LCPUFAs) and n-3 LCPUFAs, bind and activate the PPAR signaling to regulate the transcription of a cluster of genes involved in lipid and lipoprotein metabolism, FA β-oxidation in tissues with high oxidative rates, such as heart, liver, and muscle. Substrates of acyl-CoA oxidase 1 (ACOX1), the first rate-limiting peroxisomal β-oxidation enzyme, may also serve as PPARα agonists. Hydrolysis of hepatic intracellular triglyceride also yields lipid ligands for PPARa83. A range of synthetic PPARα agonists, including gemfibrozil, fenofibrate and ciprofibrate, have been synthesized and used in the treatment of primary hypertriglyceridemia or complexed dyslipidaemia84 in clinical.
Selected Functional Foods That Combat the Effects of Hyperglycemia and Chronic Inflammation
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
In a study published in the journal Chemico-Biological Interactions, it was also reported that fucoxanthin supplementation improves plasma and hepatic lipid metabolism, and blood glucose concentration, in high-fat diet–fed C57BL/6N mice: the activities of two key cholesterol regulating enzymes, acyl coenzyme A:cholesterol acyltransferase and 3-hydroxy-3-methylglutaryl coenzyme A reductase, were significantly inhibited by fucoxanthin in mice. Relative mRNA expressions of acyl-coA oxidase 1, palmitoyl (ACOX1), and peroxisome proliferator-activated receptor α (PPARα) and γ (PPARγ) were also altered in a beneficial direction by fucoxanthin in the liver (Woo, Jeon, Kim et al. 2010).
Sulfur mustard analog 2-chloroethyl ethyl sulfide increases triglycerides by activating DGAT1-dependent biogenesis and inhibiting PGC1ɑ-dependent fat catabolism in immortalized human bronchial epithelial cells
Published in Toxicology Mechanisms and Methods, 2023
Feng Ye, Qinya Zeng, Guorong Dan, Yuanpeng Zhao, Wenpei Yu, Jin Cheng, Mingliang Chen, Bin Wang, Jiqing Zhao, Yan Sai, Zhongmin Zou
Fatty acid oxidation can be summarized as activation, transportation, β-oxidation, and energy release after the product of acetyl CoA enters the tricarboxylic acid cycle to be oxidized to CO2 and H2O. PPAR and PGC1 are well-known transcription factors that regulate the expression of genes involved in fatty acid β-oxidation. Among them, mRNA and protein levels of PGC1ɑ were decreased in CEES (0.9 mM)-injured cells. Similar to another report using vesicant (Zhang et al. 2019), we also observed a decrease in Sirt1 expression, providing a possible link in regulating PGC1ɑ expression (Ventura-Clapier et al. 2008). Following application of the PGC1ɑ agonist ZLN005, TG levels in normal and CEES-injured cells were significantly reduced. Given the increased expression of PGC1β in the cytoplasm, mitochondrial biosynthesis might not be impaired. We assume that the decrease in nuclear PGC1ɑ impairs transcriptional expression of fatty acid oxidation genes, such as Acox1, Acadm, Acadv1, Cpt1b, and Pdhk4.
Administration timing and duration-dependent effects of sesamin isomers on lipid metabolism in rats
Published in Chronobiology International, 2020
Norifumi Tateishi, Satoshi Morita, Izumi Yamazaki, Hitoshi Okumura, Masaru Kominami, Sota Akazawa, Ayuta Funaki, Namino Tomimori, Tomohiro Rogi, Hiroshi Shibata, Shigenobu Shibata
It has been reported that SE reduces triglycerides in the blood and liver in rodents. As underlying the mechanisms for this action, it has been reported that SE promoted enzymatic activity and/or induced gene expression of Acox1 for beta-oxidation of fatty acids, suppressed synthesis of fatty acids by Fasn, and suppressed synthesis of triglycerides by Dgats. These enzymes are is known to be under the control of PPARα or SREBP1-c (Ashakumary et al. 1999; Ide et al. 2009; Lim et al. 2007). Many studies have been reported the relationship between metabolism of fatty acids, PPARα, circadian clock and regulation. For example, it has been shown that there is an E-box in the transcriptional regulation region of PPARα and binding with clock protein controls its transcription (Gooley 2016), giving rhythmicity to PPARα and the fatty acid metabolism enzymes that are its target genes (Guan et al. 2018; Hayashida et al. 2010; Oishi et al. 2005). Furthermore, mutations in the clock gene result in a loss of this rhythmicity in PPARα and its target genes, leading to abnormal lipid metabolism (Oishi et al. 2005; Turek et al. 2005). In recent years, these findings have been applied to conduct basic studies on the administration of PPARα agonists at times of day in a chrono-pharmacological approach (Guan et al. 2018).
Masitinib in treatment of pancreatic cancer
Published in Expert Opinion on Pharmacotherapy, 2018
Anem Waheed, Sneha Purvey, Muhammad Wasif Saif
The ACOX1 subgroups were defined using a pharmacogenomic analysis of the RNA expression in peripheral blood samples. Next generation sequencing (NGS) was performed by Acobiom in order to identify the genetic biomarker subgroup. A total of 34% of patients were identified as being ACOX1. In the ACOX1 subgroup, patients treated with combination of masitinib plus gemcitabine had a median OS of 11.7 months [95% CI (8.3–19.9)] versus 5.6 months [95% CI (3.7–12.9)] for the placebo plus gemcitabine arm. There was a statistically significant gain of 6.1 months with HR 0.23, [95% CI (0.10–0.51), p < 0.001]. Safety profile in the ACOX1 subgroup was similar to the overall population [15].