L’hyperactivité de la lipogenèse peut-elle conduire à la stéatose hépatique ?

Robichon, Céline; Girard, Jean; Postic, Catherine

doi:10.1051/medsci/20082410841

Cited by 6 publications

(5 citation statements)

References 30 publications

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“…This mechanism would explain the general decrease in fatty acid concentrations observed in our study. However, this effect could be partially counteracted by the increased xylulose 5-phosphate, which stimulates the carbohydrate responsive element binding protein, and stimulates FAS activity …”

Section: Discussionmentioning

confidence: 99%

“…However, this effect could be partially counteracted by the increased xylulose 5-phosphate, which stimulates the carbohydrate responsive element binding protein, and stimulates FAS activity. 31 Hepatic amino acid concentrations were notably decreased in PON1-deficient mice, with the exceptions of methionine sulfoxide and taurine, which were increased. Methionine sulfoxide is the oxidized form of methionine and cannot be utilized by tissues.…”

Section: Journal Of Proteome Researchmentioning

confidence: 93%

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Paraoxonase-1 Deficiency Is Associated with Severe Liver Steatosis in Mice Fed a High-fat High-cholesterol Diet: A Metabolomic Approach

et al. 2013

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Oxidative stress is a determinant of liver steatosis and the progression to more severe forms of disease. The present study investigated the effect of paraoxonase-1 (PON1) deficiency on histological alterations and hepatic metabolism in mice fed a high-fat high-cholesterol diet. We performed nontargeted metabolomics on liver tissues from 8 male PON1-deficient mice and 8 wild-type animals fed a high-fat, high-cholesterol diet for 22 weeks. We also measured 8-oxo-20-deoxyguanosine, reduced and oxidized glutathione, malondialdehyde, 8-isoprostanes and protein carbonyl concentrations. Results indicated lipid droplets in 14.5% of the hepatocytes of wild-type mice and in 83.3% of the PON1-deficient animals (P < 0.001). The metabolomic assay included 322 biochemical compounds, 169 of which were significantly decreased and 16 increased in PON1-deficient mice. There were significant increases in lipid peroxide concentrations and oxidative stress markers. We also found decreased glycolysis and the Krebs cycle. The urea cycle was decreased, and the pyrimidine cycle had a significant increase in orotate. The pathways of triglyceride and phospholipid synthesis were significantly increased. We conclude that PON1 deficiency is associated with oxidative stress and metabolic alterations leading to steatosis in the livers of mice receiving a high-fat high-cholesterol diet.

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Section: Discussionmentioning

confidence: 99%

Section: Journal Of Proteome Researchmentioning

confidence: 93%

Paraoxonase-1 Deficiency Is Associated with Severe Liver Steatosis in Mice Fed a High-fat High-cholesterol Diet: A Metabolomic Approach

et al. 2013

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“…An increase in plasma lipid can lead to a diffuse infiltration of triglycerides and fatty acid in the liver [26], causing considerable hepatocellular injury resulting in increased activity of transaminase in the serum [27]. These data could explain the significant increase in AST (55.76%) and ALT (93.13%) in mice injected with KTX 2 compared to control mice.…”

Section: Resultsmentioning

confidence: 99%

Systemic Responses following Brain Injuries and Inflammatory Process Activation Induced by a Neurotoxin of <b><i>Androctonus</i></b> Scorpion Venom

Taibi-Djennah

Matin-Eauclaire²,

Laraba-Djebari³

2015

Neuroimmunomodulation

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Objective: Kaliotoxin 2 (KTX₂), a neurotoxin isolated from Androctonus australis hector scorpion venom, presents a high affinity with the voltage-gated potassium channels. The targets of KTX₂ in the brain and its toxic effects on the cerebral cortex have been extensively studied; however, its deleterious systemic effects on other organ systems have not yet been investigated. Inflammatory response induced by KTX₂ is supported by cytokine release which could provoke multiple organ dysfunction and diverse biological disorders in mammals. The possibility that inflammatory response and brain injuries induced by KTX₂ may lead to functional disturbances, e.g. in the pancreas and the liver, were investigated. The contribution of IL-6 and TNF-α to the modulation of pathophysiological effects induced by KTX₂ was also tested. Methods: NMRI mice were injected by the intracerebroventricular route with a sublethal dose of KTX₂ or saline solution. Inflammatory response and oxidative stress were assessed in sera and tissue homogenates. Biomarkers of pancreatic and hepatic functions and the correlation with tissue damage in the brain, liver and pancreas were also analyzed. Results: The obtained results revealed that KTX₂ injection induced an inflammatory process activation and imbalanced redox status. It also induced severe alterations in cerebral cortex, hepatic and pancreatic tissues associated with a significant increase in pancreatic and hepatic pathological biomarkers. Cytokine antagonists injected 30 min prior to KTX₂ led to a significant reduction of all disturbances induced by KTX₂. Conclusion: In addition to its significant toxicity on the central nervous system, KTX₂ can also affect pancreatic and hepatic functions, probably by an indirect mechanism involving activation of the inflammatory response with release of IL-6 and TNF-α.

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“…This phenomenon is known as “ ectopic fat accumulation ” [ 20 ]. Under these conditions, the hepatocyte plasma membrane exhibits an increase in fatty acid transport proteins, such as FA-transport and FA-binding proteins, and the activation of two transcription factors, sterol regulatory element binding protein (SREBP-1c) and carbohydrate responsive element binding protein (ChREBP), which activate local de novo lipogenesis [ 21 , 22 ]. This increased hepatic lipogenesis leads to the accumulation of free fatty acids (FFAs), which are stored as TGs and exported as very low-density lipoprotein particles (VLDLs).…”

Section: Pathogenesis Of Nafldmentioning

confidence: 99%

Natural compounds proposed for the management of non-alcoholic fatty liver disease

Merenda,

Juszczak,

Ferier

et al. 2024

Nat. Prod. Bioprospect.

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Although non-alcoholic fatty liver disease (NAFLD) presents as an intricate condition characterized by a growing prevalence, the often-recommended lifestyle interventions mostly lack high-level evidence of efficacy and there are currently no effective drugs proposed for this indication. The present review delves into NAFLD pathology, its diverse underlying physiopathological mechanisms and the available in vitro, in vivo, and clinical evidence regarding the use of natural compounds for its management, through three pivotal targets (oxidative stress, cellular inflammation, and insulin resistance). The promising perspectives that natural compounds offer for NAFLD management underscore the need for additional clinical and lifestyle intervention trials. Encouraging further research will contribute to establishing more robust evidence and practical recommendations tailored to patients with varying NAFLD grades. Graphical Abstract

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L’hyperactivité de la lipogenèse peut-elle conduire à la stéatose hépatique ?

Cited by 6 publications

References 30 publications

Paraoxonase-1 Deficiency Is Associated with Severe Liver Steatosis in Mice Fed a High-fat High-cholesterol Diet: A Metabolomic Approach

Paraoxonase-1 Deficiency Is Associated with Severe Liver Steatosis in Mice Fed a High-fat High-cholesterol Diet: A Metabolomic Approach

Systemic Responses following Brain Injuries and Inflammatory Process Activation Induced by a Neurotoxin of <b><i>Androctonus</i></b> Scorpion Venom

Natural compounds proposed for the management of non-alcoholic fatty liver disease

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