Building mass to prevent non-alcoholic fatty liver disease?

Pelusi, Serena; Valenti, Luca

doi:10.21037/hbsn.2018.12.07

Cited by 6 publications

(6 citation statements)

References 13 publications

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“…Interestingly, sarcopenia was significantly associated with a higher risk for cancer‐ (HR 1.49, 95% CI 1.01‐2.20) and diabetes‐ (HR 4.94, 95% CI 1.70‐14.38) related mortality in patients with NAFLD only 20 . These findings support the notion that, in NAFLD patients with sarcopenia, physical activity and dietary interventions aimed to increase skeletal muscle mass may improve clinical outcomes 21 …”

Section: Sarcopenia and Nafld: There Is Moresupporting

confidence: 84%

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A call to action for fatty liver disease

Mantovani

Valenti

2021

Liver International

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Section: Sarcopenia and Nafld: There Is Moresupporting

confidence: 84%

“…20 These findings support the notion that, in NAFLD patients with sarcopenia, physical activity and dietary interventions aimed to increase skeletal muscle mass may improve clinical outcomes. 21…”

Section: Sarcopenia and Nafld: There Is Morementioning

confidence: 99%

A call to action for fatty liver disease

Mantovani

Valenti

2021

Liver International

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“…These data showed the effect of lifestyle in the progression and prevention of MAFLD. In fact, the most important treatment for MAFLD has been shown to be lifestyle modification [29]. The MD could be considered the gold standard in the prevention and treatment of MAFLD, and for this reason, a strict adherence to the traditional MD can help MAFLD patients in achieving a healthy state.…”

Section: Dietary Regimens In Mafldmentioning

confidence: 99%

The Many Faces of Metabolic Dysfunction-Associated Fatty Liver Disease Treatment: From the Mediterranean Diet to Fecal Microbiota Transplantation

Abenavoli,

Gambardella,

Scarlata

et al. 2024

Medicina

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The gastrointestinal tract is inhabited by the gut microbiota. The main phyla are Firmicutes and Bacteroidetes. In non-alcoholic fatty liver disease, now renamed metabolic dysfunction-associated fatty liver disease (MAFLD), an alteration in Firmicutes and Bacteroidetes abundance promotes its pathogenesis and evolution into non-alcoholic steatohepatitis, liver cirrhosis, and hepatocellular carcinoma. For this reason, early treatment is necessary to counteract its progression. The aim of the present narrative review is to evaluate the different therapeutic approaches to MAFLD. The most important treatment for MAFLD is lifestyle changes. In this regard, the Mediterranean diet could be considered the gold standard in the prevention and treatment of MAFLD. In contrast, a Western diet should be discouraged. Probiotics and fecal microbiota transplantation seem to be valid, safe, and effective alternatives for MAFLD treatment. However, more studies with a longer follow-up and with a larger cohort of patients are needed to underline the more effective approaches to contrasting MAFLD.

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“…Recent reports emphasize the importance of sirtuins in regulating metabolic processes relevant to ALD ( Kim et al, 2019 ; Ma et al, 2019 ). Ethanol exposure reduces SIRT1 gene and protein expressions ( You et al, 2015 ). Decreased SIRT1 levels play a pivotal role in ALD regulation through alterations in acetylation patterns of various target molecules, including histones, transcription regulatory factors, and co-regulatory factors ( Chang & Guarente, 2014 ; Ren et al, 2020 ; Schug & Li, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

Sirtuin 1 alleviates alcoholic liver disease by inhibiting HMGB1 acetylation and translocation

Fu,

Deng,

et al. 2023

PeerJ

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Background Alcoholic liver disease (ALD) encompasses a spectrum of liver disorders resulting from prolonged alcohol consumption and is influenced by factors such as oxidative stress, inflammation, and apoptosis. High Mobility Group Box 1 (HMGB1) plays a pivotal role in ALD due to its involvement in inflammation and immune responses. Another key factor, Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, is known for its roles in cellular stress responses and metabolic regulation. Despite individual studies on HMGB1 and SIRT1 in ALD, their specific molecular interactions and combined effects on disease advancement remain incompletely understood. Methods Alcohol-induced liver injury (ALI) models were established using HepG2 cells and male C57BL/6 mice. HMGB1 and SIRT1 expressions were assessed at the mRNA and protein levels usingreverse transcription-quantitative polymerase chain reaction, western blot, and immunofluorescence staining. The physical interaction between HMGB1 and SIRT1 was investigated using co-immunoprecipitation and immunofluorescence co-expression analyses. Cellular viability was evaluated using the CCK-8 assay. Results In patients with clinical ALI, HMGB1 mRNA levels were elevated, while SIRT1 expression was reduced, indicating a negative correlation between the two. ALI models were successfully established in cells and mice, as evidenced by increased markers of cellular and liver damage. HMGB1 acetylation and translocation were observed in both ALI cells and mouse models. Treatment with the SIRT1 agonist, SRT1720, reversed the upregulation of HMGB1 acetylation, nuclear translocation, and release in the ethyl alcohol (EtOH) group. Furthermore, SIRT1 significantly attenuated ALI. Importantly, in vivo binding was confirmed between SIRT1 and HMGB1. Conclusions SIRT1 alleviates HMGB1 acetylation and translocation, thereby ameliorating ALI.

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Building mass to prevent non-alcoholic fatty liver disease?

Cited by 6 publications

References 13 publications

A call to action for fatty liver disease

A call to action for fatty liver disease

The Many Faces of Metabolic Dysfunction-Associated Fatty Liver Disease Treatment: From the Mediterranean Diet to Fecal Microbiota Transplantation

Sirtuin 1 alleviates alcoholic liver disease by inhibiting HMGB1 acetylation and translocation

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