Non‐alcoholic fatty liver disease: raising awareness of a looming public health problem

Author(s):  
Lucy Gracen ◽  
Elizabeth E Powell
2009 ◽  
Vol 116 (7) ◽  
pp. 539-564 ◽  
Author(s):  
Christopher D. Byrne ◽  
Rasaq Olufadi ◽  
Kimberley D. Bruce ◽  
Felino R. Cagampang ◽  
Mohamed H. Ahmed

NAFLD (non-alcoholic fatty liver disease) refers to a wide spectrum of liver damage, ranging from simple steatosis to NASH (non-alcoholic steatohepatitis), advanced fibrosis and cirrhosis. NAFLD is strongly associated with insulin resistance and is defined by accumulation of liver fat >5% per liver weight in the presence of <10 g of daily alcohol consumption. The exact prevalence of NAFLD is uncertain because of the absence of simple non-invasive diagnostic tests to facilitate an estimate of prevalence. In certain subgroups of patients, such as those with Type 2 diabetes, the prevalence of NAFLD, defined by ultrasound, may be as high as 70%. NASH is an important subgroup within the spectrum of NAFLD that progresses over time with worsening fibrosis and cirrhosis, and is associated with increased risk for cardiovascular disease. It is, therefore, important to understand the pathogenesis of NASH and, in particular, to develop strategies for interventions to treat this condition. Currently, the ‘gold standard’ for the diagnosis of NASH is liver biopsy, and the need to undertake a biopsy has impeded research in subjects in this field. Limited results suggest that the prevalence of NASH could be as high as 11% in the general population, suggesting there is a worsening future public health problem in this field of medicine. With a burgeoning epidemic of diabetes in an aging population, it is likely that the prevalence of NASH will continue to increase over time as both factors are important risk factors for liver fibrosis. The purpose of this review is to: (i) briefly discuss the epidemiology of NAFLD to describe the magnitude of the future potential public health problem; and (ii) to discuss extra- and intra-hepatic mechanisms contributing to the pathogenesis of NAFLD, a better understanding of which may help in the development of novel treatments for this condition.


2021 ◽  
Author(s):  
Dandan Shan ◽  
Jinming Wang ◽  
Qiannan Di ◽  
Qianqian Jiang ◽  
Qian Xu

Non-alcoholic fatty liver disease (NAFLD) has increasingly become a serious public health problem. There is growing evidence that nonylphenol (NP) exposure may cause steatosis, but the underlying mechanism is not...


2019 ◽  
Vol 78 (3) ◽  
pp. 290-304 ◽  
Author(s):  
J. Bernadette Moore

Non-alcoholic fatty liver disease (NAFLD) is now a major public health concern with an estimated prevalence of 25–30% of adults in many countries. Strongly associated with obesity and the metabolic syndrome, the pathogenesis of NAFLD is dependent on complex interactions between genetic and environmental factors that are not completely understood. Weight loss through diet and lifestyle modification underpins clinical management; however, the roles of individual dietary nutrients (e.g. saturated and n-3 fatty acids; fructose, vitamin D, vitamin E) in the pathogenesis or treatment of NAFLD are only partially understood. Systems biology offers valuable interdisciplinary methods that are arguably ideal for application to the studying of chronic diseases such as NAFLD, and the roles of nutrition and diet in their molecular pathogenesis. Although present in silico models are incomplete, computational tools are rapidly evolving and human metabolism can now be simulated at the genome scale. This paper will review NAFLD and its pathogenesis, including the roles of genetics and nutrition in the development and progression of disease. In addition, the paper introduces the concept of systems biology and reviews recent work utilising genome-scale metabolic networks and developing multi-scale models of liver metabolism relevant to NAFLD. A future is envisioned where individual genetic, proteomic and metabolomic information can be integrated computationally with clinical data, yielding mechanistic insight into the pathogenesis of chronic diseases such as NAFLD, and informing personalised nutrition and stratified medicine approaches for improving prognosis.


2021 ◽  
pp. 24-25
Author(s):  
Ruby Kumari ◽  
Prof. Santosh Kumar ◽  
Debarshi Jana

Background: NAFLD is a major alarming public health problem in current scenario. Still there is lack of wide research data in context of NAFLD, in our institute and state (Jharkhand) so we felt the need to do this research to assess dyslipidemia in cases of NAFLD. 100 Material and methods: patients (18-70 yrs) age Group, were included in the study. 50 diagnosed cases of Fatty Liver disease (FLD) by USG were enrolled in study. Subjects were divided in two equal groups, NAFLD and controls. Lipid prole was done in both groups. Data obtained during research was Result: statistically analyzed by using SPSS version 20. Student t test for independent samples was used to determine statistical signicance, p-value <0.05 was considered statistically signicant. serum Triglyceride, serum LDL-C and VLDL-C was signicantly raised and HDL-C signicantly decreased in NAFLD group compared to control. Dyslipidemia was obtained in NA Conclusion: FLD group.


2021 ◽  
Vol 22 (13) ◽  
pp. 6900
Author(s):  
Aleksandra Hliwa ◽  
Bruno Ramos-Molina ◽  
Dariusz Laski ◽  
Adriana Mika ◽  
Tomasz Sledzinski

Non-alcoholic fatty liver disease (NAFLD) is a major public health problem worldwide. NAFLD (both simple steatosis and steatohepatitis) is characterized by alterations in hepatic lipid metabolism, which may lead to the development of severe liver complications including cirrhosis and hepatocellular carcinoma. Thus, an exhaustive examination of lipid disorders in the liver of NAFLD patients is much needed. Mass spectrometry-based lipidomics platforms allow for in-depth analysis of lipid alterations in a number of human diseases, including NAFLD. This review summarizes the current research on lipid alterations associated with NAFLD and related complications, with special emphasis on the changes in long-chain and short-chain fatty acids levels in both serum and liver tissue, as well as in the hepatic expression of genes encoding the enzymes catalyzing lipid interconversions.


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