Current Treatment of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis

Hung, Chun Kit; Bodenheimer, Henry C.

doi:10.1016/j.cld.2017.08.012

Cited by 28 publications

(22 citation statements)

References 83 publications

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“…The consumption of coffee is related to a decreased risk of cirrhosis, hepatocellular carcinoma, and mortality [ 150 ]. Several studies have observed that regular coffee intake is significantly associated with reduced hepatic fibrosis of NAFLD [ 151 , 152 ].…”

Section: Treatment Of Lipotoxic Liver Injurymentioning

confidence: 99%

New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis

Méndez-Sánchez

Cruz-Ramón

Ramírez-Pérez

et al. 2018

IJMS

123

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NASH is becoming increasingly common worldwide because of the growing global prevalence of obesity and consequently NAFLD. Unfortunately, the mechanism of progression of NAFLD to NASH and then cirrhosis is not completely understood. Several factors, including insulin resistance, inflammation, oxidative stress, lipotoxicity, and bile acid (BA) toxicity, have been reported to be associated with NASH progression. The release of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, which is caused by the ectopic accumulation of triglyceride-derived toxic metabolites and the subsequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis. Adipose tissue (AT), especially visceral AT, comprises multiple cell populations that produce adipokines and insulin-like growth factor, plus macrophages and other immune cells that stimulate the development of lipotoxic liver disease. These biomolecules have been recently linked with many digestive diseases and gastrointestinal malignancies such as hepatocellular carcinoma. This made us question what role lipotoxicity has in the natural history of liver fibrosis. Therefore, this review focuses on the close relationship between AT and NASH. A good comprehension of the pathways that are related to dysregulated AT, metabolic dysfunction, and hepatic lipotoxicity will result in the development of prevention strategies and promising therapeutics for patients with NASH.

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Section: Treatment Of Lipotoxic Liver Injurymentioning

confidence: 99%

New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis

Méndez-Sánchez

Cruz-Ramón

Ramírez-Pérez

et al. 2018

IJMS

123

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show abstract

“…Studies have evaluated the effects of nutraceuticals as a co-adjuvant treatment for NAFLD and cardiovascular complications. In some clinical trials, nutraceuticals were found to ameliorate the liver function and histology [17]. L-carnitine (LC) is an essential nutrient that converts fats into energy in the mitochondrion and plays an important role in lipid metabolism.…”

Section: Introductionmentioning

confidence: 99%

L-carnitine supplementation attenuates NAFLD progression and cardiac dysfunction in a mouse model fed with methionine and choline-deficient diet

Mollica

Senesi

Codella

et al. 2020

Digestive and Liver Disease

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Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disorder. NAFLD, associated lipotoxicity, fibrosis, oxidative stress, and altered mitochondrial metabolism, is responsible for systemic inflammation, which contributes to organ dysfunction in extrahepatic tissues, including the heart. We investigated the ability of L-carnitine (LC) to oppose the pathogenic mechanisms underlying NAFLD progression and associated heart dysfunction, in a mouse model of methionine-choline-deficient diet (MCDD). Mice were divided into three groups: namely, the control group (CONTR) fed with a regular diet and two groups fed with MCDD for 6 weeks. In the last 3 weeks, one of the MCDD groups received LC (200 mg/kg each day) through drinking water (MCDD + LC). The hepatic lipid accumulation and oxidative stress decreased after LC supplementation, which also reduced hepatic fibrosis via modulation of ␣-smooth muscle actin (␣SMA), peroxisome-activated receptor gamma (PPAR␥), and nuclear factor kappa B (Nf B) expression. LC ameliorated systemic inflammation, mitigated cardiac reactive oxygen species (ROS) production, and prevented fibrosis progression by acting on signal transducer and activator of transcription 3 (STAT3), extracellular signal-regulated kinase 1-2 (ERK1-2), and ␣SMA. This study confirms the existence of a relationship between fatty liver disease and cardiac abnormalities and highlights the role of LC in controlling liver oxidative stress, steatosis, fibrosis, and NAFLD-associated cardiac dysfunction.

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“…There is no definitive treatment for NAFLD . The current clinical therapies focus on improving the metabolic parameters involved in NAFLD pathogeneses, including weight loss, decreasing IR, lowering oxidative stress, and modulating blood glucose levels .…”

Section: Introductionmentioning

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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Current Treatment of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis

Cited by 28 publications

References 83 publications

New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis

New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis

L-carnitine supplementation attenuates NAFLD progression and cardiac dysfunction in a mouse model fed with methionine and choline-deficient diet

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

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