Hydrogen sulphide in liver glucose/lipid metabolism and non‐alcoholic fatty liver disease

Mateus, Inês; Prip‐Buus, Carina

doi:10.1111/eci.13680

Cited by 12 publications

(5 citation statements)

References 101 publications

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“…Thereby by, a significant improvement has been observed regarding albumin, ammonia, ALP, AST, ALT, HR, troponin I, LDH, and CK-MB serum levels following their administration with a more relevant improvement has been observed following NaHS administration when compared with the control group (I). In line with our observed results, (Ertugrul et al 2021 ; Guo et al 2020 ; Yang et al 2021 ; Sun et al 2021 ; Mateus and Prip-Buus 2022 ) proved the efficiency of the administration of exogenous hydrogen sulphide donor and MSCs in alleviating cardiac and liver dysfunctions by promoting tissue regeneration, inhibiting fibrosis, and regulating immune responses.…”

Section: Discussionsupporting

confidence: 89%

Hepatic and cardiac implications of increased toxic amyloid-beta serum level in lipopolysaccharide-induced neuroinflammation in rats: new insights into alleviating therapeutic interventions

Anwar

Mabrouk

2023

Inflammopharmacol

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Neuroinflammation is a devastating predisposing factor for Alzheimer’s disease (AD). A number of clinical findings have reported peripheral disorders among AD patients. Amyloid beta (Aβ) is a toxic physiological aggregate that serves as a triggering factor for hepatic and cardiac disorders related to neurotoxicity. As a drawback of Aβ excessive accumulation in the brain, part of Aβ is believed to readily cross the blood–brain barrier (BBB) into the peripheral circulation resulting in serious inflammatory and toxic cascades acting as a direct bridge to cardiac and hepatic pathophysiology. The main aim is to find out whether neuroinflammation-related AD may result in cardiac and liver dysfunctions. Potential therapeutic interventions are also suggested to alleviate AD’s cardiac and hepatic defects. Male rats were divided into: control group I, lipopolysaccharide (LPS)-neuroinflammatory-induced group II, LPS-neuroinflammatory-induced group treated with sodium hydrogen sulphide donor (NaHS) (group III), and LPS-neuroinflammatory-induced group treated with mesenchymal stem cells (MSCs) (group IV). Behavior and histopathological studies were conducted in addition to the estimation of different biological biomarkers. It was revealed that the increased toxic Aβ level in blood resulted in cardiac and hepatic malfunctions as a drawback of exaggerated inflammatory cascades. The administration of NaHS and MSCs proved their efficiency in combating neuroinflammatory drawbacks by hindering cardiac and hepatic dysfunctions. The consistent direct association of decreased heart and liver functions with increased Aβ levels highlights the direct involvement of AD in other organ complications. Thereby, these findings will open new avenues for combating neuroinflammatory-related AD and long-term asymptomatic toxicity. Graphic abstract

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Section: Discussionsupporting

confidence: 89%

Hepatic and cardiac implications of increased toxic amyloid-beta serum level in lipopolysaccharide-induced neuroinflammation in rats: new insights into alleviating therapeutic interventions

Anwar

Mabrouk

2023

Inflammopharmacol

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“…Recently, it was shown that this model of simple fatty liver in female rats also presented reduced hepatic H 2 S production, with BemA treatment restoring the biosynthesis of this gasotransmitter [36 & ]. Other in-vivo and in-vitro models of NAFLD show impaired hepatic H 2 S synthesis, with H 2 S donor treatment being effective in reducing hepatic steatosis and NASHrelated features [37]. Therefore, the increase in H 2 S production caused by BemA treatment may be an additional mechanism contributing to ameliorate hepatic steatosis [36 & ].…”

Section: Bempedoic Acid and Nafld: Results In Animal Models And Propo...mentioning

confidence: 99%

Bempedoic acid for nonalcoholic fatty liver disease: evidence and mechanisms of action

Roglans

Laguna

Alegret

2023

Current Opinion in Lipidology

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Purpose of review Nonalcoholic fatty liver disease (NAFLD) is a highly prevalent progressive condition that lacks a specific pharmacological treatment. ATP-citrate lyase (ACLY) is one of the emergent targets for the treatment of NAFLD. This review aims to summarize the role of ACLY in NAFLD, provide evidence of the beneficial effects of the ACLY inhibitor bempedoic acid (BemA) in NAFLD and discuss the mechanisms involved. Recent findings BemA is effective in reducing hepatic steatosis in several animal models that recapitulate different stages of the disease. Thus, in a dietary model of simple hepatic steatosis in female rats, BemA abrogates the accumulation of liver fat. Apart from ACLY inhibition, BemA has several functions in the liver that contribute to the antisteatotic effect: inhibition of ketohexokinase, induction of patatin-like phospholipase domain-containing protein 3 and increases in both fatty acid β-oxidation activity and hepatic H2S production. In models of the advanced phases of NAFLD, BemA reduces not only steatosis, but also ballooning, lobular inflammation and hepatic fibrosis, by mechanisms involving both hepatocytes and hepatic stellate cells. Summary BemA, an ACLY inhibitor currently approved for the treatment of hypercholesterolemia, may be a useful drug to treat NAFLD through its antisteatotic, anti-inflammatory and antifibrotic effects.

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“…In the presented work, we show that the administration of BemA to female Sprague-Dawley rats fed an HFD supplemented with a 10% w/v fructose solution as a beverage (HFHFr diet) reverses the decreased production of liver H 2 S induced by consumption of the HFHFr diet. As H 2 S has a prominent role in the regulation of liver glucose and triglyceride metabolism [22], the recovery of liver H 2 S production induced by BemA could contribute to the recently described therapeutic effect of BemA in several experimental models of NAFLD [18,23].…”

Section: Discussionmentioning

confidence: 99%

Bempedoic Acid Restores Liver H2S Production in a Female Sprague-Dawley Rat Dietary Model of Non-Alcoholic Fatty Liver

Roglans

Fauste

Bentanachs

et al. 2022

IJMS

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We previously demonstrated that treatment with BemA (bempedoic acid), an inhibitor of ATP citrate lyase, significantly reduces fatty liver in a model of liver steatosis (HFHFr—female Sprague-Dawley rat fed a high-fat high-fructose diet). Since the hepatic production of the gasotransmitter H2S is impaired in liver disorders, we were interested in determining if the production of H2S was altered in our HFHFr model and whether the administration of BemA reversed these changes. We used stored liver samples from a previous study to determine the total and enzymatic H2S production, as well as the expression of CBS (cystathionine β-synthase), CSE (cystathionine γ-lyase), and 3MST (3-mercaptopiruvate sulfurtransferase), and the expression/activity of FXR (farnesoid X receptor), a transcription factor involved in regulating CSE expression. Our data show that the HFHFr diet reduces the total and enzymatic production of liver H2S, mainly by decreasing the expression of CBS and CSE. Furthermore, BemA treatment restored H2S production, increasing the expression of CBS and CSE, providing evidence for the involvement of FXR transcriptional activity and the mTORC1 (mammalian target of rapamycin1)/S6K1 (ribosomal protein S6 kinase beta-1)/PGC1α (peroxisome proliferator receptor gamma coactivator1α) pathway.

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Hydrogen sulphide in liver glucose/lipid metabolism and non‐alcoholic fatty liver disease

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cited by 12 publications

References 101 publications

Hepatic and cardiac implications of increased toxic amyloid-beta serum level in lipopolysaccharide-induced neuroinflammation in rats: new insights into alleviating therapeutic interventions

Hepatic and cardiac implications of increased toxic amyloid-beta serum level in lipopolysaccharide-induced neuroinflammation in rats: new insights into alleviating therapeutic interventions

Bempedoic acid for nonalcoholic fatty liver disease: evidence and mechanisms of action

Bempedoic Acid Restores Liver H2S Production in a Female Sprague-Dawley Rat Dietary Model of Non-Alcoholic Fatty Liver

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