scholarly journals The Epidemiology, Risk Profiling and Diagnostic Challenges of Nonalcoholic Fatty Liver Disease

Medicines ◽  
2019 ◽  
Vol 6 (1) ◽  
pp. 41 ◽  
Author(s):  
Umair Iqbal ◽  
Brandon Perumpail ◽  
Daud Akhtar ◽  
Donghee Kim ◽  
Aijaz Ahmed
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
High Risk ◽  
Environmental Factors ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Active Management ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of liver damage from the more prevalent (75%–80%) and nonprogressive nonalcoholic fatty liver (NAFL) category to its less common and more ominous subset, nonalcoholic steatohepatitis (NASH). NAFLD is now the most common cause of chronic liver disease in the developed world and is a leading indication for liver transplantation in United States (US). The global prevalence of NAFLD is estimated to be 25%, with the lowest prevalence in Africa (13.5%) and highest in the Middle East (31.8%) and South America (30.4%). The increasing incidence of NAFLD has been associated with the global obesity epidemic and manifestation of metabolic complications, including hypertension, diabetes, and dyslipidemia. The rapidly rising healthcare and economic burdens of NAFLD warrant institution of preventative and treatment measures in the high-risk sub-populations in an effort to reduce the morbidity and mortality associated with NAFLD. Genetic, demographic, clinical, and environmental factors may play a role in the pathogenesis of NAFLD. While NAFLD has been linked with various genetic variants, including PNPLA-3, TM6SF2, and FDFT1, environmental factors may predispose individuals to NAFLD as well. NAFLD is more common in older age groups and in men. With regards to ethnicity, in the US, Hispanics have the highest prevalence of NAFLD, followed by Caucasians and then African-Americans. NAFLD is frequently associated with the components of metabolic syndrome, such as type 2 diabetes mellitus (T2DM), obesity, hypertension, and dyslipidemia. Several studies have shown that the adoption of a healthy lifestyle, weight loss, and pro-active management of individual components of metabolic syndrome can help to prevent, retard or reverse NAFLD-related liver damage. Independently, NAFLD increases the risk of premature cardiovascular disease and associated mortality. For this reason, a case can be made for screening of NAFLD to facilitate early diagnosis and to prevent the hepatic and extra-hepatic complications in high risk sub-populations with morbid obesity, diabetes, and other metabolic risk factors.

scholarly journals Differences in metabolic and liver pathobiology induced by two dietary mouse models of nonalcoholic fatty liver disease

2020 ◽  
Vol 319 (5) ◽  
pp. E863-E876
Author(s):  
Hannah Zhang ◽  
Mélissa Léveillé ◽  
Emilie Courty ◽  
Aysim Gunes ◽  
Bich N. Nguyen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Liver Cancer ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Chow Diet ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic linked to metabolic disease. The first stage of NAFLD is characterized by lipid accumulation in hepatocytes, but this can progress into nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). Western diets, high in fats, sugars, and cholesterol, are linked to NAFLD development. Murine models are often used to study NAFLD; however, there remains debate on which diet-induced model best mimics both human disease progression and pathogenesis. In this study, we performed a side-by-side comparison of two popular diet models of murine NAFLD/NASH and associated HCC, a high-fat diet supplemented with 30% fructose water (HFHF) and a Western diet high in cholesterol (WDHC), and these were compared with a common grain-based chow diet (GBD). Mice on both experimental diets developed liver steatosis, and WDHC-fed mice had greater levels of hepatic inflammation and fibrosis than HFHF-fed mice. In contrast, HFHF-fed mice were more obese and developed more severe metabolic syndrome, with less pronounced liver disease. Despite these differences, WDHC-fed and HFHF-fed mice had similar tumor burdens in a model of diet-potentiated liver cancer. Response to diet and resulting phenotypes were generally similar between sexes, albeit delayed in females. This study shows that modest differences in diet can significantly uncouple glucose homeostasis and liver damage. In conclusion, long-term feeding of either HFHF or WDHC is a reliable method to induce NASH and diet-potentiated liver cancer in mice of both sexes; however, the choice of diet involves a trade-off between severity of metabolic syndrome and liver damage.

NR1H4 rs35724 G>C Variant Modulates Liver Damage in Nonalcoholic Fatty Liver Disease

2020 ◽  
Author(s):  
Stefania Grimaudo ◽  
Paola Dongiovanni ◽  
Jussi Pihlajamäki ◽  
Mohammed Eslam ◽  
Hannele Yki-Järvinen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver

scholarly journals Multidisciplinary Pharmacotherapeutic Options for Nonalcoholic Fatty Liver Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Kei Nakajima
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Lipid Lowering ◽  
Nonalcoholic Fatty Liver ◽  
Ras Blockers

Nonalcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are multidisciplinary liver diseases that often accompany type 2 diabetes or metabolic syndrome, which are characterized by insulin resistance. Therefore, effective treatment of type 2 diabetes and metabolic syndrome should target not only the cardiometabolic abnormalities, but also the associated liver disorders. In the last decade, it has been shown that metformin, thiazolidinediones, vitamin E, ezetimibe, n-3 polyunsaturated fatty acids, renin-angiotensin system (RAS) blockers, and antiobesity drugs may improve hepatic pathophysiological disorders as well as clinical parameters. Accordingly, insulin sensitizers, antioxidative agents, Niemann-Pick C1-like 1 (NPC1L1) inhibitors, RAS blockers, and drugs that target the central nervous system may represent candidate pharmacotherapies for NAFLD and possibly NASH. However, the efficacy, safety, and tolerability of long-term treatment (potentially for many years) with these drugs have not been fully established. Furthermore, clinical trials have not comprehensively examined the efficacy of lipid-lowering drugs (i.e., statins, fibrates, and NPC1L1 inhibitors) for the treatment of NAFLD. Although clinical evidence for RAS blockers and incretin-based agents (GLP-1 analogs and dipeptidyl peptidase-4 inhibitors) is also lacking, these agents are promising in terms of their insulin-sensitizing and anti-inflammatory effects without causing weight gain.

NR1H4 rs35724 G>C Variant Modulates Liver Damage in Nonalcoholic Fatty Liver Disease

2021 ◽  
Author(s):  
Stefania Grimaudo ◽  
Paola Dongiovanni ◽  
Jussi Pihlajamäki ◽  
Mohammed Eslam ◽  
Hannele Yki‐Järvinen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver

scholarly journals Metabolic syndrome and severity of fibrosis in nonalcoholic fatty liver disease: An age-dependent risk profiling study

2017 ◽  
Vol 37 (9) ◽  
pp. 1389-1396 ◽  
Author(s):  
Salvatore Petta ◽  
Mohammed Eslam ◽  
Luca Valenti ◽  
Elisabetta Bugianesi ◽  
Marco Barbara ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Risk Profiling ◽  
Age Dependent
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