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Nonalcoholic Fatty Liver Disease
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Fat accumulation in the liver also can be stimulated by fructose consumption inducing oxidative stress in the mitochondria. Acontinase-2 and enoyl CoA hydrase are enzymes found in the mitochondria that are sensitive to oxidative stress (Jensen et al. 2018). Fructose and uric acid decrease acontinase-2 activity, leading to the accumulation of citrate, which moves into the cytoplasm, stimulates ATP citrate lyase, and activates lipogenesis (Jensen et al. 2018). This can also impair fatty acid oxidation by decreasing enoyl CoA hydratase-1 activity, which stimulates AMP Deaminase-2 and reduces AMP-activated protein kinase, which regulates enoyl CoA hydratase-1. This results in accumulation of fat and stimulation of gluconeogenesis (Jensen et al. 2018).
Biochemical Aspects of Fatty Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
In any case, oxidation occurs after preliminary activation of FFA to acyl-CoA derivatives. As acyl-CoAs cannot cross the mitochondrial membrane, they must be first transformed in acyl-carnitines, which are able to penetrate across these membranes. Inside mitochondria, acyl-carnitines react with CoA to reform acyl-CoAs, whereas carnitine can return to the cytoplasm to renew its shuttle work. Acyl-CoAs are now ready to be oxidized on the internal mitochondrial membrane. The oxidizing system is composed by several enzymes. The first attack is produced by acyl-CoA dehydrogenases, which contain FAD. Resulting enoyl-CoAs are then hydrated by specific enoyl-CoA hydratase, producing β-hydroxyacy1-CoAs.
Lower-intensity aerobic endurance sports
Published in Nick Draper, Helen Marshall, Exercise Physiology, 2014
In the second reaction of β oxidation the addition of water hydrates the transenoyl CoA molecule to form 3-hydroxyacyl CoA; this is catalysed by the enzyme enoyl CoA hydratase. The third reaction is similar to the first in that the enzyme, in this case 3-hydroxyacyl CoA dehydrogenase, catalyses the removal of two hydrogen atoms, but the carrier in this instance is NAD+. In the final reaction, CoA is attached to the final two carbon atoms during their split from the acyl CoA molecule, creating acetyl CoA. This reaction is catalysed by acyl CoA thiolase. The newly formed acetyl CoA molecule is then available to enter Krebs cycle while the new acyl CoA molecule re-enters the β oxidation cycle. For the process of β oxidation to continue, FAD and NAD+ must be regenerated. This occurs through the transfer of electrons from FADH2 and NADH to the electron transport chain. In common with the Krebs cycle and the ETC, therefore, β oxidation is an oxygen-dependent process.
Fructose and hepatic insulin resistance
Published in Critical Reviews in Clinical Laboratory Sciences, 2020
Samir Softic, Kimber L. Stanhope, Jeremie Boucher, Senad Divanovic, Miguel A. Lanaspa, Richard J. Johnson, C. Ronald Kahn
As discussed above, when fructose is metabolized by KHK, there is a transient decrease in intracellular ATP that activates the nucleotide degradation pathway and subsequent uric acid formation [74,75]. A central role of uric acid in mediating fructose effects is inferred from studies demonstrating that it further stimulates KHK expression in a fast-forward loop, which accelerates fructose metabolism [35]. Furthermore, uric acid can also play a part in increasing lipogenesis and decreasing beta-oxidation. Uric acid blocks enoyl-CoA hydratase and decreases AMPK activation, thus contributing to fructose-induced decrease in FAO [76]. It also can stimulate lipogenesis by inducing NADPH oxidase, which associates with the mitochondria, resulting in oxidative stress that reduces aconitase-2, leading to generation of citrate, a lipogenic precursor [60,75]. In addition to being produced by fructose metabolism, uric acid may stimulate endogenous fructose production by activating aldose reductase in the polyol pathway, which drives development of NAFLD [77].
The role of radiation induced oxidative stress as a regulator of radio-adaptive responses
Published in International Journal of Radiation Biology, 2020
Mohsen Sisakht, Maryam Darabian, Amir Mahmoodzadeh, Ali Bazi, Sayed Mohammad Shafiee, Pooneh Mokarram, Zahra Khoshdel
The balance between oxidant-redox species following radiation is further regulated by alternations in the gene expression pattern. Nuclear factor erythroid 2-related factor 2 (Nrf2), also known as heme-binding protein 1 (HEBP1), is a transcription factor suggested to be critical in determining the redox balance following radiation (gamma; 5 Gy) (Khan et al. 2015). A cysteine-rich cytoplasmic protein, Kelch-like ECH (enoyl-CoA hydratase)-associated protein 1 (Keap1), has been identified as an activator of Nrf2 in the presence of oxidative stress (Anuranjani and Bala 2014; Luo et al. 2014). Also, the perturbation of Nrf2 signaling pathway can lead to unbalanced oxidative-redox state. In fact, Nrf2 gene gain-of-function mutations promoted antioxidant responses in the tumor cells irradiated with 8 Gy X-ray (Schaue et al. 2015).
Prognostic significance of proteomics and multi-omics studies in renal carcinoma
Published in Expert Review of Proteomics, 2020
Francesca Raimondo, Marina Pitto
Very recently, a study was published on 18 pairs of RCC and ANK frozen tissues, from patients grouped according to the stage [28]. Using iTRAQ-based proteomics analysis, authors identified 130 differentially expressed proteins, but none of them allowed discriminating among different tumor stages, apart from enoyl-CoA hydratase, short chain 1 (ECHS1), a key enzyme in fatty acid metabolism, whose downregulation in RCC tissues discriminated stage I from ANK tissues (AUROC> 0.7). Although ECHS1 did not give any prognostic information, it was identified as a tumor suppressor, as its overexpression in RCC cultured cells inhibited proliferation and migration through inhibiting mTOR pathway activation [28].