Treatment of Non-Alcoholic Fatty Liver Disease

Dyson, Jessica; Day, Chris

doi:10.1159/000360511

Cited by 42 publications

(34 citation statements)

References 96 publications

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“…Liver-specific therapeutic interventions such as thiazolidinedione pharmacotherapy could pose specific benefit in non-cirrhotic NASH [44] . There is still however insufficient evidence to justify the routine clinical use of any specific targeted treatments at this time.…”

Section: Composite Diagnostic Models For Nashmentioning

confidence: 99%

Composite prognostic models across the non-alcoholic fatty liver disease spectrum: Clinical application in developing countries

Luckhoff

Kruger

Kotze

2015

WJH

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Heterogeneity in clinical presentation, histological severity, prognosis and therapeutic outcomes charac teristic of nonalcoholic fatty liver disease (NAFLD) necessitates the development of scientifically sound classification schemes to assist clinicians in stratifying patients into meaningful prognostic subgroups. The need for replacement of invasive liver biopsies as the standard method whereby NAFLD is diagnosed, graded and staged with biomarkers of histological severity injury led to the development of composite prognostic models as potentially viable surrogate alternatives. In the present article, we review existing scoring systems used to (1) confirm the presence of undiagnosed hepatosteatosis; (2) distinguish between simple steatosis and NASH; and (3) predict advanced hepatic fibrosis, with particular emphasis on the role of NAFLD as an independent cardiometabolic risk factor. In addition, the incorporation of functional genomic markers and application of emerging imaging technologies are discussed as a means to improve the diagnostic accuracy and predictive performance of promising composite models found to be most appropriate for widespread clinical adoption. Composite prognostic models across the non-alcoholic fatty liver disease spectrum: Clinical application in developing countries have entered the clinical domain as potentially viable alternatives. Lifestylebased intervention remains the cornerstone of treatment in patients with NAFLD. The widespread clinical adoption of composite diagnostic and predictive models could however prove useful in informing clinical and therapeutic decision making with the goal of adding value to patient care across the NAFLD spectrum.Lückhoff HK, Kruger FC, Kotze MJ. Composite prognostic models across the non-alcoholic fatty liver disease spectrum:

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Section: Composite Diagnostic Models For Nashmentioning

confidence: 99%

Composite prognostic models across the non-alcoholic fatty liver disease spectrum: Clinical application in developing countries

Luckhoff

Kruger

Kotze

2015

WJH

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“…NAFLD is the most common liver disorder, affecting 20%-30% of the adult population and more than 80% of obese people in the world. NAFLD can develop into nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (2). As a component of metabolic syndrome, NAFLD is tightly associated with insulin resistance, type 2 diabetes, coronary heart disease, and atherosclerosis (3).…”

Section: Introductionmentioning

confidence: 99%

Intestinal farnesoid X receptor signaling promotes nonalcoholic fatty liver disease

Jiang¹,

Xie²,

Li³

et al. 2014

J. Clin. Invest.

569

513

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. measured for 8 days. The feces were collected every 2 days for 8 days. Ileal and fecal lipids were extracted as described in the Supplemental Methods. Triglycerides were measured with a triglyceride colorimetric assay kit (Bioassay Systems). Free fatty acids (FFAs) were measured using reagents from Wako.Statistics. Experimental values are presented as the mean ± SD. Statistical analyses were performed using the 2-tailed Student's t test and 1-way ANOVA with Tukey's confirmation. Weighted UniFrac analysis to assess changes in bacterial abundance was performed on the Galaxy web-based platform. Statistical models including PCA, PLS-DA, and OPLS-DA were established to represent the major latent variables in the data matrix. P values of less than 0.05 were considered significant. Study approval. All animal studies were performed in accordance with the Institute of Laboratory Animal Resources guidelines and approved by the IACUC of the NCI.

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“…Nonalcoholic fatty liver disease (NAFLD) is a spectrum of diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), which may progress to cirrhosis. NAFLD is strongly associated with insulin resistance, and up to 50% of NAFLD patients have type 2 diabetes (Dyson & Day 2014). A significant proportion of patients with cirrhosis ranging between 35 and 80% may be insulin resistant, and 20-30% of patients may be clinically diabetic (Ahmadieh & Azar 2014).…”

Section: Introductionmentioning

confidence: 99%

Metformin improves hepatic IRS2/PI3K/Akt signaling in insulin-resistant rats of NASH and cirrhosis

Hong

Zhou

Liu

et al. 2016

Journal of Endocrinology

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Nonalcoholic fatty liver disease and cirrhosis are strongly associated with insulin resistance and glucose intolerance. To date, the influence of metformin on glycogen synthesis in the liver is controversial. Limited studies have evaluated the effect of metformin on hepatic insulin signaling pathway in vivo. In this study, an insulin-resistant rat model of nonalcoholic steatohepatitis and cirrhosis was developed by high-fat and high-sucrose diet feeding in combination with subcutaneous injection of carbon tetrachloride. Liver tissues of the model rats were featured with severe steatosis and cirrhosis, accompanied by impaired liver function and antioxidant capacity. The glucose tolerance was impaired, and the index of insulin resistance was increased significantly compared with the control. The content of hepatic glycogen was dramatically decreased. The expression of insulin receptor β (IRβ); phosphorylations of IRβ, insulin receptor substrate 2 (IRS2), and Akt; and activities of phosphatidylinositol 3-kinase (PI3K) and glycogen synthase (GS) in the liver were significantly decreased, whereas the activities of glycogen synthase kinase 3α (GSK3α) and glycogen phosphorylase a (GPa) were increased. Metformin treatment remarkably improved liver function, alleviated lipid peroxidation and histological damages of the liver, and ameliorated glucose intolerance and insulin resistance. Metfromin also significantly upregulated the expression of IRβ; increased the phosphorylations of IRβ, IRS2, and Akt; increased the activities of PI3K and GS; and decreased GSK3α and GPa activities. In conclusion, our study suggests that metformin upregulates IRβ expression and the downstream IRS2/PI3K/Akt signaling transduction, therefore, to increase hepatic glycogen storage and improve insulin resistance. These actions may be attributed to the improved liver histological alterations by metformin.

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Treatment of Non-Alcoholic Fatty Liver Disease

Cited by 42 publications

References 96 publications

Composite prognostic models across the non-alcoholic fatty liver disease spectrum: Clinical application in developing countries

Composite prognostic models across the non-alcoholic fatty liver disease spectrum: Clinical application in developing countries

Intestinal farnesoid X receptor signaling promotes nonalcoholic fatty liver disease

Metformin improves hepatic IRS2/PI3K/Akt signaling in insulin-resistant rats of NASH and cirrhosis

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