Role of histone deacetylase on nonalcoholic fatty liver disease

S, Fu; Yu, Meihong; Tan, Yuyong; Liu, Dengliang

doi:10.1080/17474124.2021.1854089

Cited by 7 publications

(11 citation statements)

References 98 publications

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“…HDAC1, 2, and 3 are reported to be protective against NAFLD, while HDAC7, 8, and 11 promote NAFLD. 49 In the present study, all animals were administered the same set of chemical drugs, which reduced the possibility that the chemicals used to induce IS in these rats affected signaling pathways studied in this investigation. As far as we are aware, there is no evidence showing intracerebral injection of doxorubicin and lipopolysaccharide affects the hepatic pathways reported here.…”

Section: Discussionmentioning

confidence: 99%

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Probiotics counteract hepatic steatosis caused by ketogenic diet and upregulate AMPK signaling in a model of infantile epilepsy

Nikpoor

Tompkins

et al. 2022

eBioMedicine

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Background Infantile spasms syndrome (IS) is a type of epilepsy affecting 1.6 to 4.5 per 10,000 children in the first year of life, often with severe lifelong neurodevelopmental consequences. Only two first-line pharmacological treatments currently exist for IS and many children are refractory to these therapies. In such cases, children are treated with the ketogenic diet (KD). While effective in reducing seizures, the diet can result in dyslipidemia over time.Methods Employing a neonatal Sprague-Dawley rat model of IS, we investigated how the KD affects hepatic steatosis and its modulation by a defined probiotic blend. A combination of multiple readouts, including malondialdehyde, fatty acid profiles, lipid metabolism-related enzyme mRNA expression, mitochondrial function, histone deacetylase activity, cytokines and chemokines were evaluated using liver homogenates.Findings The KD reduced seizures, but resulted in severe hepatic steatosis, characterized by a white liver, triglyceride accumulation, elevated malondialdehyde, polyunsaturated fatty acids and lower acyl-carnitines compared to animals fed a control diet. The KD-induced metabolic phenotype was prevented by the co-administration of a blend of Streptococcus thermophilus HA-110 and Lactococcus lactis subsp. lactis HA-136. This probiotic blend protected the liver by elevating pAMPK-mediated signaling and promoting lipid oxidation. The strains further upregulated the expression of caspase 1 and interleukin 18, which may contribute to their hepatoprotective effect in this model.Interpretation Our results suggest that early intervention with probiotics could be considered as an approach to reduce the risk of hepatic side effects of the KD in children who are on the diet for medically indicated reasons.

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Section: Discussionmentioning

confidence: 99%

“…HDAC1, 2, and 3 are reported to be protective against NAFLD, while HDAC7, 8, and 11 promote NAFLD. 49 …”

Section: Discussionmentioning

confidence: 99%

Probiotics counteract hepatic steatosis caused by ketogenic diet and upregulate AMPK signaling in a model of infantile epilepsy

Nikpoor

Tompkins

et al. 2022

eBioMedicine

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“…In latest years, epigenetic modifications in DNA and histone have been studied as essential mechanisms that modify the development of liver diseases including MAFLD. Hence the dysregulation of epigenetic modifications has a critical role in MAFLD progression since it regulates the expression and activity of various genes implicated in lipid metabolism, insulin resistance, DNA repair, and inflammatory process that enhance the pathogenesis of MAFLD ( 10 , 131 ). Currently, it has been demonstrated that miRNAs involved in lipid synthesis, fatty acid, and glucose catabolism and inflammation are dysregulated in MAFLD being useful as biomarkers ( 132 ).…”

Section: Discussionmentioning

confidence: 99%

An Update in Epigenetics in Metabolic-Associated Fatty Liver Disease

et al. 2022

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Metabolic-associated fatty liver disease (MAFLD) is characterized by hepatic steatosis accompanied by one of three features: overweight or obesity, T2DM, or lean or normal weight with evidence of metabolic dysregulation. It is distinguished by excessive fat accumulation in hepatocytes, and a decrease in the liver's ability to oxidize fats, the accumulation of ectopic fat, and the activation of proinflammatory pathways. Chronic damage will keep this pathophysiologic cycle active causing progression from hepatic steatosis to cirrhosis and eventually, hepatocarcinoma. Epigenetics affecting gene expression without altering DNA sequence allows us to study MAFLD pathophysiology from a different perspective, in which DNA methylation processes, histone modifications, and miRNAs expression have been closely associated with MAFLD progression. However, these considerations also faced us with the circumstance that modifying those epigenetics patterns might lead to MAFLD regression. Currently, epigenetics is an area of great interest because it could provide new insights in therapeutic targets and non-invasive biomarkers. This review comprises an update on the role of epigenetic patterns, as well as innovative therapeutic targets and biomarkers in MAFLD.

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“…[5,40] In the recent decade, extensive studies from animal models and human patients have found that NAFLD disease progression is closely associated with bile acid dysregulation and sphingolipid homeostasis. [48][49][50][51][52][53][54][55][56][57][58][59][60] Mechanisms linking bile acid metabolism to the development of NAFLD Consistently, clinical studies have demonstrated that primary and secondary CBAs are tightly associated with NAFLD progression and NASH severity. [30,48,49,51,52] A recent study reported that elevated hepatic taurochenodeoxycholic acid (TCDCA) and taurocholic acid (TCA) in NAFLD patients was associated with symptom onset, disease progression, or death.…”

Section: Bile Acids and Sphingolipids In Nafldmentioning

confidence: 99%

“…[57] HDACs have been recently recognized as important pathogenetic players in NAFLD. [58] However, due to the broad regulator effect on gene transcription, targeting HDACs alone may not be feasible as the treatment for NAFLD. [58] Since the identification of FXR as the first bile acid nuclear receptor and TGR5 as the first bile acid-activated GPCR, extensive studies have been done to examine the therapeutic potential for NAFLD by modulating FXR and TGR5 activity.…”

Section: Bile Acids and Sphingolipids In Nafldmentioning

confidence: 99%

Bile acids and sphingolipids in non-alcoholic fatty liver disease

Jackson

Way

Zhou

2022

Chinese Medical Journal

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Non-alcoholic fatty liver disease (NAFLD) is one of the fastest-growing diseases, and its global prevalence is estimated to increase >50% by 2030. NAFLD is comorbid with metabolic syndrome, obesity, type 2 diabetes, and insulin resistance. Despite extensive research efforts, there are no pharmacologic or biological therapeutics for the treatment of NAFLD. Bile acids and sphingolipids are well-characterized signaling molecules. Over the last few decades, researchers have uncovered potential mechanisms by which bile acids and sphingolipids regulate hepatic lipid metabolism. Dysregulation of bile acid and sphingolipid metabolism has been linked to steatosis, inflammation, and fibrosis in patients with NAFLD. This clinical observation has been recapitulated in animal models, which are well-accepted by experts in the hepatology field. Recent transcriptomic and lipidomic studies also show that sphingolipids are important players in the pathogenesis of NAFLD. Moreover, the identification of bile acids as activators of sphingolipid-mediated signaling pathways established a novel theory for bile acid and sphingolipid biology. In this review, we summarize the recent advances in the understanding of bile acid and sphingolipid-mediated signaling pathways as potential contributors to NAFLD. A better understanding of the pathologic effects mediated by bile acids and sphingolipids will facilitate the development of new diagnostic and therapeutic strategies for NAFLD.

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Role of histone deacetylase on nonalcoholic fatty liver disease

Cited by 7 publications

References 98 publications

Probiotics counteract hepatic steatosis caused by ketogenic diet and upregulate AMPK signaling in a model of infantile epilepsy

Probiotics counteract hepatic steatosis caused by ketogenic diet and upregulate AMPK signaling in a model of infantile epilepsy

An Update in Epigenetics in Metabolic-Associated Fatty Liver Disease

Bile acids and sphingolipids in non-alcoholic fatty liver disease

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