Role of peroxisome proliferator-activated receptors in non-alcoholic fatty liver disease inflammation

Silva, Amanda Karolina Soares; Peixoto, Christina Alves

doi:10.1007/s00018-018-2838-4

Cited by 72 publications

(55 citation statements)

References 123 publications

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“…It has been suggested that OEA modulates food intake by increasing feeding latency, promoting control of energy intake, decreasing meal size, and increasing the intervals between meals by boosting the expression of genes associated with satiety . The major action of OEA in regulating food intake is mediated by PPAR‐α activation, an important transcriptional regulator of energy balance and fat metabolism . OEA is considered to be a high‐affinity PPAR‐α agonist .…”

Section: Major Mechanisms Of Action Of Oea In the Management Of Nafldmentioning

confidence: 99%

The effects of oleoylethanolamide, an endogenous PPAR‐α agonist, on risk factors for NAFLD: A systematic review

et al. 2019

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Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease.Recently, some novel compounds have been investigated for the prevention and treatment of NAFLD. Oleoylethanolamide (OEA), an endogenous PPAR-α agonist, has exhibited a plethora of pharmacological properties for the treatment of obesity and other obesity-associated metabolic complications. This systematic review was performed with a focus on the effects of OEA on the risk factors for NAFLD.PubMed, Scopus, Embase, ProQuest, and Google Scholar databases were searched up to December 2018 using relevant keywords. All articles written in English evaluating the effects of OEA on the risk factors for NAFLD were eligible for the review. The evidence reviewed in this article illustrates that OEA regulates multiple biological processes associated with NAFLD, including lipid metabolism, inflammation, oxidative stress, and energy homeostasis through different mechanisms. In summary, many beneficial effects of OEA have led to the understanding that OEA may be an effective therapeutic strategy for the management of NAFLD. Although a wide range of studies have demonstrated the most useful effects of OEA on NAFLD and the associated risk factors, further clinical trials, from both in vivo studies and in vitro experiments, are warranted to verify these outcomes.

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Section: Major Mechanisms Of Action Of Oea In the Management Of Nafldmentioning

confidence: 99%

The effects of oleoylethanolamide, an endogenous PPAR‐α agonist, on risk factors for NAFLD: A systematic review

et al. 2019

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“…Pparg encodes the peroxisome‐proliferator‐activated receptor that is involved in the transcriptional regulation of lipid metabolism 37 and has been defined as a steatogenic factor 38 . Fabp2 and Cd36 encode membrane‐associated fatty acid‐binding proteins (fatty acid transporters) that facilitate and regulate cellular fatty acid uptake, 39 whereas Mogat1 is involved in an alternative pathway for triglyceride synthesis contributing to the development of hepatic steatosis, especially obesity‐related steatosis 40,41 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of the variability in the extent of nonalcoholic fatty liver induced by a high‐fat diet in the genetically diverse Collaborative Cross mouse model

et al. 2020

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Interindividual variability and sexual dimorphisms in the development of nonalcoholic fatty liver disease (NAFLD) are still poorly understood. In the present study, male and female strains of Collaborative Cross (CC) mice were fed a high‐fat and high‐sucrose (HF/HS) diet or a control diet for 12 weeks to investigate interindividual‐ and sex‐specific variations in the development of NAFLD. The severity of liver steatosis varied between sexes and individual strains and was accompanied by an elevation of serum markers of insulin resistance, including increases in total cholesterol, low‐density lipoproteins, high‐density lipoproteins, phospholipids, and glucose. The development of NAFLD was associated with overexpression of the critical fatty acid uptake and de novo lipogenesis genes Pparg, Mogat1, Cd36, Acaab1, Fabp2, and Gdf15 in male and female mice. The expression of Pparg, Mogat1, and Cd36 was positively correlated with liver triglycerides in male mice, and Mogat1 and Cd36 expression were positively correlated with liver triglycerides in female mice. Our results indicate the value of CC mice in combination with HF/HS diet‐induced alterations as an approach to study the susceptibility and interindividual variabilities in the pathogenesis of nonalcoholic fatty liver and early nonalcoholic steatohepatitis at the population level, uncovering of susceptible and resistant cohorts, and identifying sex‐specific molecular determinants of disease susceptibility.

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“…PPARα activation induces the increase in fatty acid oxidation, ketogenesis and gluconeogenesis [32]. PPARβ/δ activation exerts regulatory effects on fatty acid catabolism, reverse cholesterol transport and energy metabolism, and even reduces insulin resistance and plasma glucose [33]. PPARγ shifts lipids from non-adipose organs such as the liver and skeletal muscles to white adipose tissue, leading to the attenuation of lipotoxicity [34].…”

Section: Discussionmentioning

confidence: 99%

Identify Key Active Ingredients and Molecular Mechanisms of Jiangzhi Decoction on Non-alcoholic Fatty Liver Disease by Network Pharmacology Analysis

Wang

Zhi

et al. 2020

Preprint

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Background: Jiangzhi Decoction (JZD), a traditional herb mixture, has shown significant clinical efficacy against non-alcoholic fatty liver disease (NAFLD). However, its multicomponent and multitarget characteristics bring difficulty in deciphering its pharmacological mechanisms. Our study aimed to identify the key active ingredients and core molecular mechanisms of JZD against NAFLD. Methods: The active ingredients were searched from Traditional Chinese Medicine Systems Pharmacology (TCMSP) database and Traditional Chinese Medicine Integrated Database (TCMID). The targets of those ingredients were identified using ChemMapper database based on 3D-structure similarity. NAFLD-related genes were searched from DisGeNET database and Gene Expression Omnibus (GEO) database. Then we obtained candidate targets of JZD against NAFLD by overlapping the active ingredient targets and NAFLD-related genes. We performed protein-protein interaction (PPI) analysis, functional enrichment analysis and constructed pathway networks of “herbs-active ingredients-candidate targets”, and identified the key active ingredients and core molecular mechanisms in the network. Results: We found 147 active ingredients in JZD, 1285 targets of active ingredients, 401 NAFLD-related genes, and 59 overlapped candidate targets of JZD against NAFLD. 22 core targets were obtained by PPI analysis. Finally, nuclear receptor transcription and lipid metabolism regulation were found as the core molecular mechanisms of JZD against NAFLD by functional enrichment analysis, and emodin, emodin anthrone, hyperin, questin, rhein, etc. were speculated as the key active ingredients of JZD. Conclusion: Our study will provide the scientific evidences of the clinical efficacy of JZD against NAFLD.

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Role of peroxisome proliferator-activated receptors in non-alcoholic fatty liver disease inflammation

Cited by 72 publications

References 123 publications

The effects of oleoylethanolamide, an endogenous PPAR‐α agonist, on risk factors for NAFLD: A systematic review

The effects of oleoylethanolamide, an endogenous PPAR‐α agonist, on risk factors for NAFLD: A systematic review

Characterization of the variability in the extent of nonalcoholic fatty liver induced by a high‐fat diet in the genetically diverse Collaborative Cross mouse model

Identify Key Active Ingredients and Molecular Mechanisms of Jiangzhi Decoction on Non-alcoholic Fatty Liver Disease by Network Pharmacology Analysis

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