Can NASH lipidome provide insight into the pathogenesis of obesity-related non-alcoholic fatty liver disease?

Birerdinc, Aybike; Younossi, Zobair M.

doi:10.1016/j.jhep.2015.01.005

Cited by 9 publications

(5 citation statements)

References 12 publications

(13 reference statements)

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“…In the present study, we provide evidence of a protective role of CREG in NAFLD. Despite recent research, the treatment strategies and mechanism underlying the complicated pathological processes of NAFLD remain unclear . After researching CREG for more than 10 years, our laboratory has found that CREG is a suppressor of various cardiovascular diseases with a basic function in promoting cell differentiation and inhibiting cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

The novel intracellular protein CREG inhibits hepatic steatosis, obesity, and insulin resistance

Zhang

Zhao

Tian³

et al. 2017

Hepatology

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The results of our study provides evidence that CREG is a robust suppressor of hepatic steatosis and metabolic disorders through its direct interaction with ASK1 and the resultant inactivation of ASK1-JNK1 signaling. This study offers insights into NAFLD pathogenesis and its complicated pathologies, such as obesity and insulin resistance, and paves the way for disease treatment through targeting CREG. (Hepatology 2017;66:834-854).

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Section: Discussionmentioning

confidence: 99%

The novel intracellular protein CREG inhibits hepatic steatosis, obesity, and insulin resistance

Zhang

Zhao

Tian³

et al. 2017

Hepatology

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“…NASH is multifactorial and is considered to be the hepatic manifestation of metabolic syndrome, which is a major harmful factor for numerous diseases. 31 Currently, there is no proven effective therapy for NASH. Thus, the development of new drugs for NASH therapy is necessary.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of glycyrrhizic acid from edible botanical glycyrrhiza glabra against non-alcoholic steatohepatitis in mice

et al. 2016

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Non-alcoholic steatohepatitis (NASH) is a syndrome with simultaneous severe hepatic steatosis, lobular inflammation and pericelluar fibrosis. The purpose of the present study is to investigate the protective effect of glycyrrhizic acid (GA), a natural triterpene glycoside from edible botanical glycyrrhiza glabra, on NASH induced by a methionine and choline-deficient (MCD) diet in mice, and further to elucidate the mechanisms of GA protection. Serum ALT and AST assay and H&E staining were used to identify the amelioration of the liver histopathological changes. Serum and hepatic lipid assay and Oil Red O staining were used to measure lipid accumulation. Hepatic inflammatory and fibrosis gene determination, as well as Mason Trichrome and Sirius Red staining were used to determine the reduction of hepatic inflammation and pericelluar fibrosis. Quantitative real-time PCR and Western blot assays were used to elucidate the mechanisms underlying GA protection. The results indicated that GA treatment reduced hepatic lipogenesis through a decrease in hepatic levels of SREBP-1c, FAS, ACC1 and SCD1, and increased lipid metabolism through an induction of PPARα, CPT1α, ACADS and LPL. GA also reduced hepatic inflammation via a decrease in the expression of the hepatic inflammatory genes MCP-1 and VCAM-1. In addition, GA reduced liver fibrosis through limiting HSC activation and collagen deposition. In conclusion, GA produces a markedly protective effect against NASH induced by a methionine and choline-deficient (MCD) diet in mice.

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“…Nonalcoholic fatty liver disease (NAFLD) is a prevalent noninfectious chronic liver disease with an estimated global occurrence of about 20-30%, becoming one of the most important causes of liver disease worldwide [1][2][3]. This global burden, which is intimately due to an unhealthy lifestyle, represents simple steatosis to steatohepatitis, cirrhosis, and even hepatocellular carcinoma [1,4].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Linked Organ Lipid Hydroperoxidation and Dysregulation in Mouse Model of Nonalcoholic Steatohepatitis: Revealed by Lipidomic Profiling of Liver and Kidney

Chen

Fuda

et al. 2021

Antioxidants

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Nonalcoholic steatohepatitis (NASH) is a prevalent disease related to lipid metabolism disorder and oxidative stress. Lipid hydroperoxidation is known to be a critical driving force of various disorders and diseases. However, the combination of both intact and hydroperoxidized lipids in NASH has not yet been studied. In this work, the liver and kidney samples from NASH-model mice were comprehensively investigated by using the LC/MS-based lipidomic analysis. As a result, triglycerides showed the amount accumulation and the profile alteration for the intact lipids in the NASH group, while phosphatidylethanolamines, lysophosphatidylethanolamines, plasmalogens, and cardiolipins largely depleted, suggesting biomembrane damage and mitochondria dysfunction. Notably, the lipid hydroperoxide species of triglyceride and phosphatidylcholine exhibited a significant elevation in both the liver and the kidney of the NASH group and showed considerable diagnostic ability. Furthermore, the relationship was revealed between the lipid metabolism disturbance and the lipid hydroperoxide accumulation, which played a key role in the vicious circle of NASH. The present study suggested that the omics approach to the lipid hydroperoxide profile might be the potential diagnostic marker of NASH and other oxidative stress-related diseases, as well as the evaluative treatment index of antioxidants.

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Can NASH lipidome provide insight into the pathogenesis of obesity-related non-alcoholic fatty liver disease?

Cited by 9 publications

References 12 publications

The novel intracellular protein CREG inhibits hepatic steatosis, obesity, and insulin resistance

The novel intracellular protein CREG inhibits hepatic steatosis, obesity, and insulin resistance

Protective effects of glycyrrhizic acid from edible botanical glycyrrhiza glabra against non-alcoholic steatohepatitis in mice

Oxidative Stress Linked Organ Lipid Hydroperoxidation and Dysregulation in Mouse Model of Nonalcoholic Steatohepatitis: Revealed by Lipidomic Profiling of Liver and Kidney

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