Concise review of lipidomics in nonalcoholic fatty liver disease

Béland-Bonenfant, Sarah; Rouland, Alexia; Petit, Jean‐Michel; Vergès, Bruno

doi:10.1016/j.diabet.2023.101432

Cited by 14 publications

(11 citation statements)

References 48 publications

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“…Interestingly, changes in LPC in the context of NAFLD/NASH might be related to LPC acyltransferase activity. In the study of Béland-Bonenfant et al, the circulating lipid profiles of 679 patients were examined, analyzing over 400 lipid species to predict hepatic fat content and NAFLD, concluding to lower LPC levels, especially C16:0 and C18:0 for NAFLD patients [29,31]. This observation aligns with our study, where we found significantly lower hepatic levels of LPC 18:0, highlighting the potential relevance of this LPC as a biomarker for NAFLD.…”

Section: Discussionsupporting

confidence: 90%

“…Moreover, diminished concentrations of PCs abundant in PUFAs, specifically those containing FA 22:6, are also evident in NAFLD. The observed decline in the conversion of PE to PC likely signifies a reduction in production via the methionine cycle, impacting the synthesis of S-adenosylmethionine (SAM), which is essential for the enzymatic conversion of PE to PC [29].…”

Section: Discussionmentioning

confidence: 99%

“…The rise in palmitoleic acid (FA 16:1n7), coupled with lower stearic acid (FA 18:0), suggests enhanced ∆9 stearoyl-CoA desaturase activity, consistent with our findings. The increase in palmitoleic acid might represent an adaptive anti-inflammatory reaction to counteract the pro-inflammatory effects of fatty acid overload [29]. Increased dietary intake of ω-6 polyunsaturated fatty acids has raised the ω-6 to ω-3 ratio, contributing to NAFLD.…”

Section: Discussionmentioning

confidence: 99%

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Lipidomic Analysis of Liver and Adipose Tissue in a High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease Mice Model Reveals Alterations in Lipid Metabolism by Weight Loss and Aerobic Exercise

Mouskeftara,

Deda,

Papadopoulos

et al. 2024

Molecules

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Detailed investigation of the lipidome remodeling upon normal weight conditions, obesity, or weight loss, as well as the influence of physical activity, can help to understand the mechanisms underlying dyslipidemia in metabolic conditions correlated to the emergence and progression of non-alcoholic fatty liver disease (NAFLD). C57BL/6 male mice were fed a normal diet (ND) or a high-fat diet (HFD) for 20 weeks. Subgroups within the high-fat diet (HFD) group underwent different interventions: some engaged in exercise (HFDex), others were subjected to weight loss (WL) by changing from the HFD to ND, and some underwent a combination of weight loss and exercise (WLex) during the final 8 weeks of the 20-week feeding period. To support our understanding, not only tissue-specific lipid remodeling mechanisms but also the cross-talk between different tissues and their impact on the systemic regulation of lipid metabolism are essential. Exercise and weight loss-induced specific adaptations in the liver and visceral adipose tissue lipidomes of mice were explored by the UPLC–TOF–MS/MS untargeted lipidomics methodology. Lipidomic signatures of ND and HFD-fed mice undergoing weight loss were compared with animals with and without physical exercise. Several lipid classes were identified as contributing factors in the discrimination of the groups by multivariate analysis models, such as glycerolipids, glycerophospholipids, sphingolipids, and fatty acids, with respect to liver samples, whereas triglycerides were the only lipid class identified in visceral adipose tissue. Lipids found to be dysregulated in HFD animals are related to well-established pathways involved in the biosynthesis of PC, PE, and TG metabolism. These show a reversing trend back to basic levels of ND when animals change to a normal diet after 12 weeks, whereas the impact of exercise, though in some cases it slightly enhances the reversing trend, is not clear.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Lipidomic Analysis of Liver and Adipose Tissue in a High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease Mice Model Reveals Alterations in Lipid Metabolism by Weight Loss and Aerobic Exercise

Mouskeftara,

Deda,

Papadopoulos

et al. 2024

Molecules

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show abstract

Section: Introductionmentioning

confidence: 99%

“…palmitic acid [PA; C16:0] and stearic acid [SA; C18:0]) free cholesterol, and ceramides. 5 This abnormal cellular lipid composition, so-called lipotoxicity, eventually leads to organelle dysfunction, chronic inflammation, and apoptosis of the hepatocytes, hallmarks strongly associated with NAFLD progression to NASH. 6 Apart from lipotoxicity, SFAs trigger pro-inflammatory responses by binding to and activating damage-associated molecular pattern receptors including Toll-like receptor-4 (TLR4).…”

Section: Introductionmentioning

confidence: 99%

Saturated fatty acid-enriched small extracellular vesicles mediate a crosstalk inducing liver inflammation and hepatocyte insulin resistance

García-Martínez¹,

Alén²,

Pereira³

et al. 2023

JHEP Reports

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Lipid Nanoparticle‐Mediated Delivery of CRISPR‐Cas9 Against Rubicon Ameliorates NAFLD by Modulating CD36 Along with Glycerophospholipid Metabolism

Bai,

Nan,

et al. 2024

Advanced Science

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Non‐alcoholic fatty liver disease (NAFLD) is a prominent cause of various chronic metabolic hepatic diseases with limited therapeutics. Rubicon, an essential regulator in lysosomal degradation, is reported to exacerbate hepatic steatosis in NAFLD mice and patients, indicating its probability of being a therapeutic target for NAFLD treatment. In this study, the therapeutic potential of Rubicon blockage is investigated. Lipid nanoparticles carrying Rubicon‐specific CRISPR‐Cas9 components exhibited liver accumulation, cell internalization, and Rubicon knockdown. A single administration of the nanoparticles results in attenuated lipid deposition and hepatic steatosis, with lower circulating lipid levels and decreased adipocyte size in NAFLD mice. Furthermore, the increase of phosphatidylcholine and phosphatidylethanolamine levels can be observed in the NAFLD mice livers after Rubicon silencing, along with regulatory effects on metabolism‐related genes such as CD36, Gpcpd1, Chka, and Lpin2. The results indicate that knockdown of Rubicon improves glycerophospholipid metabolism and thereby ameliorates the NAFLD progression, which provides a potential strategy for NAFLD therapy via the restoration of Rubicon.

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Concise review of lipidomics in nonalcoholic fatty liver disease

Cited by 14 publications

References 48 publications

Lipidomic Analysis of Liver and Adipose Tissue in a High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease Mice Model Reveals Alterations in Lipid Metabolism by Weight Loss and Aerobic Exercise

Lipidomic Analysis of Liver and Adipose Tissue in a High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease Mice Model Reveals Alterations in Lipid Metabolism by Weight Loss and Aerobic Exercise

Saturated fatty acid-enriched small extracellular vesicles mediate a crosstalk inducing liver inflammation and hepatocyte insulin resistance

Lipid Nanoparticle‐Mediated Delivery of CRISPR‐Cas9 Against Rubicon Ameliorates NAFLD by Modulating CD36 Along with Glycerophospholipid Metabolism

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