Gene/Protein Disease Symptom Drug Enzyme Compound
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 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease in both adults and children worldwide. As a disease spectrum, NAFLD may progress from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. An estimated 20-35% of the general population has steatosis, 10% of whom will develop the more progressive non-alcoholic steatohepatitis associated with markedly increased risk of cardiovascular- and liver-related mortality. Development of NAFLD is strongly linked to components of the metabolic syndrome including obesity, insulin resistance, dyslipidaemia and type 2 diabetes. The recognition that NAFLD is an independent risk factor for CVD is a major public health concern. There is a great need for a sensitive non-invasive test for the early detection and assessment of the stage of NAFLD that could also be used to monitor response to treatment. The cellular and molecular aetiology of NAFLD is multi-factorial; genetic polymorphisms influencing NAFLD have been identified and nutrition is a modifiable environmental factor influencing NAFLD progression. Weight loss through diet and exercise is the primary recommendation in the clinical management of NAFLD. The application of systems biology to the identification of NAFLD biomarkers and factors involved in NAFLD progression is an area of promising research.
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PMID:Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome. 2015 39

Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver damage, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), 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 <10g of daily alcohol consumption. The exact prevalence of NAFLD is uncertain because of the absence of simple noninvasive diagnostic tests to facilitate an estimate of prevalence but in subgroups of people such as those with type 2 diabetes, the prevalence 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 NASH is associated with increased risk for cardiovascular disease. It is, therefore, important to understand the pathogenesis of NASH specifically, to develop strategies for interventions to treat this condition. The purpose of this review is to discuss the roles of inflammation, fatty acids and fatty acids in nutrition, in the pathogenesis and potential treatment of NAFLD.
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PMID:Fatty liver: role of inflammation and fatty acid nutrition. 2018 87

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of hepatic dysfunction encountered in general practice. A large proportion of individuals with type 2 diabetes and the metabolic syndrome develop NAFLD. NAFLD is associated with severe insulin resistance and increased risk of cardiovascular disease and can progress to non-alcoholic steato-hepatitis, liver cirrhosis and cancer. Currently the only known effective treatments for NAFLD are lifestyle changes including stable weight loss and a diet low in calories. General practitioners will increasingly play a key role in dealing with this evolving but serious epidemic of NAFLD and associated metabolic complications. However, success will depend on the appropriate systems and mechanisms being in place in primary care and the proper motivation, support and education of the patient. This review provides the primary care physician with: (a) a step-by step guide of how to identify NAFLD, (b) information to exclude common other causes of liver fat accumulation and (c) additional insight into relationships between NAFLD and other conditions such as obesity, cardiovascular disease and type 2 diabetes.
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PMID:Non-Alcoholic Fatty Liver Disease (NAFLD): new challenge for general practitioners and important burden for health authorities? 2029 94

Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent causes of hepatic dysfunction and is highly correlated with components of the metabolic syndrome such as obesity, insulin resistance and type 2 diabetes. Among others, nutritional factors, physical inactivity, genetic variants and visceral obesity have been identified as risk parameters for NAFLD. The complex pathophysiology of fatty liver degeneration, however, and especially the interaction between hepatocytes and adipose tissue has not been completely elucidated. Furthermore, it is not entirely understood whether insulin resistance generates fatty liver disease or vice versa. Nevertheless, adipocytokines are likely to be involved in the pathogenesis of NAFLD since they are secreted not only from adipose tissue but also from the liver. For several adipocytokines such as leptin, adiponectin, tumor necrosis factor-alpha, retinol binding protein 4 (RBP4) or fetuin-A a crucial role in the development and progression of fatty liver disease has been suggested. It has been accepted that obesity is an independent risk factor for NAFLD. Dysregulation of adipocytokines may represent an important mechanism linking increased fat mass in obesity with the development of fatty liver disease. Here, we discuss the association of RBP4 and other recently discovered adipocytokines and their relation with NAFLD.
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PMID:Retinol-binding protein 4 and new adipocytokines in nonalcoholic fatty liver disease. 2037 Jun 70

Nonalcoholic fatty liver disease (NAFLD) refers to a spectrum of liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis and cirrhosis. NAFLD is considered the hepatic component of the metabolic syndrome and insulin resistance represents its pathophysiological hallmark. Insulin resistance in NAFLD is characterized by reduced whole-body, hepatic, and adipose tissue insulin sensitivity. The mechanism(s) underlying the accumulation of fat in the liver may include excess dietary fat, increased delivery of free fatty acids to the liver, inadequate fatty acid oxidation, and increased de novo lipogenesis. Liver fat is highly correlated with all the components of the metabolic syndrome, independent of obesity, and NAFLD may increase the risk of type 2 diabetes and atherosclerosis. Overproduction of glucose, very low-density lipoproteins, C-reactive protein and coagulation factors by the fatty liver could contribute to the excess risk of cardiovascular disease. The reason(s) why some patients will develop NASH are poorly understood. Circulating free fatty acids may be cytotoxic by inducing lipid peroxidation and hepatocyte apoptosis. Insulin resistance is often associated with chronic low-grade inflammation, and numerous mediators released from immune cells and adipocytes may contribute liver damage and liver disease progression. Understanding the molecular mediators of liver injury would promote the development of mechanism-based therapeutic interventions. This article briefly summarizes the recent advances in our understanding of the relationship between NAFLD/NASH, insulin resistance and the metabolic syndrome.
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PMID:Insulin resistance in nonalcoholic fatty liver disease. 2037 Jun 77

Nonalcoholic fatty liver disease (NAFLD) is a rapidly emerging chronic liver disease and is reported to affect up to 70-80% of overweight and obese individuals. NAFLD represents a spectrum of liver diseases that range from simple hepatic steatosis, to a more severe and treatment resistant stage that features steatosis plus inflammation, termed nonalcoholic steatohepatitis (NASH), which may in turn progress to hepatic fibrosis, cirrhosis, and sub-acute liver failure. Thus, NAFLD and its subsequent complications create a significant health burden, and currently there is no effective treatment strategy. The biochemical mechanisms that underlie NAFLD are unclear at this time, but there is evidence that insulin resistance is a major contributing factor. In addition, circulating concentrations of inflammatory cytokines (e.g., TNF-alpha, IL-6) as well as decreased antiinflammatory factors (e.g., adiponectin, IL-10) are not only implicated in the development of insulin resistance and type 2 diabetes, but are also related to NAFLD. Such inflammatory mechanisms are fundamental in the progression of NAFLD toward higher risk cirrhotic states. This review outlines the leading theories of pathogenesis of NAFLD and highlights the potential role of exercise in treating and preventing NAFLD. Regular exercise can reverse insulin resistance, suppress low-grade systemic inflammation, and attenuate inflammatory markers associated with NAFLD. Thus, exercise has the potential to become an effective treatment and prevention modality for NAFLD and NASH.
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PMID:Nonalcoholic fatty liver disease: biochemical and therapeutic considerations. 2038 43

Non-alcoholic fatty liver represents one of the most prevalent conditions affecting about one third of the general population in the Western world, and its prevalence is continuously increasing parallel to the epidemics of obesity. Non-alcoholic fatty liver is a strong predictor of non-alcoholic steatohepatitis, but also of cirrhosis, end-stage liver disease and hepatocellular carcinoma. In recent years, non-alcoholic fatty liver (in addition to overall and visceral obesity) has emerged as a risk factor for insulin resistance, hypertension, dyslipidemia, cardiovascular events and type 2 diabetes. This review summarizes the information currently available about the mechanisms involved in liver fat accumulation (e.g. hepatic lipid supply, de novo lipogenesis, lipid oxidation and the packaging and secretion of triglycerides in the form of very-low-density lipoproteins). New aspects concerning mechanisms potentially leading to a 'dissociation' of fatty liver and insulin resistance are also discussed. Understanding the pathogenesis of fatty liver and its complications, including the identification of new factors secreted from the liver under excess fat accumulation that are involved in the regulation of metabolism ('hepatokines'), is crucial in order to develop and implement efficient prevention and treatment strategies.
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PMID:Environmental and genetic determinants of fatty liver in humans. 2046 Sep 7

Over the last few years, the paradigm in hepatology has changed from focusing on a single liver disease to considering concurrent diseases, in particular obesity and related metabolic factors. Obesity has reached epidemic proportions globally and is associated with insulin resistance, steatosis and a low-grade systemic inflammatory state. These metabolic factors have a synergistic role in the natural history and treatment outcomes related to chronic liver disease. This is characterized best in chronic hepatitis C where steatosis and insulin resistance are caused by viral and metabolic effects. Non-alcoholic fatty liver disease and related metabolic abnormalities also exacerbate other diseases, such as alcoholic liver disease and haemochromatosis. In addition, there is growing evidence linking obesity and type 2 diabetes with hepatocellular carcinoma in subjects with chronic viral hepatitis. The pathogenesis of co-morbid disease may be related to increased oxidative stress, inflammatory injury and cell death, along with altered hepatocyte regeneration and repair. Hyperinsulinaemia and other metabolic factors may also have a direct role in the progression of liver injury. Data indicate that weight reduction improves steatosis and inflammation in patients with chronic hepatitis C. This has important clinical and therapeutic implications and suggests that obesity should be actively addressed in the management of patients with other chronic liver diseases.
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PMID:Metabolic factors and non-alcoholic fatty liver disease as co-factors in other liver diseases. 2046 Sep 9

Non-alcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance, and its prevalence is rising in parallel with worldwide increases in obesity and type 2 diabetes. However, the nature of this relationship remains debatable. In particular, it is unclear whether insulin resistance causes NAFLD or hepatic steatosis per se reduces insulin sensitivity. This review will examine data from recent studies on the link between insulin resistance and NAFLD, focusing on studies that have attempted to dissociate fatty liver and hepatic insulin resistance.
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PMID:Interrelationships between hepatic fat and insulin resistance in non-alcoholic fatty liver disease. 2070 85

Nonalcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD) share common features. Both are associated with visceral obesity, type 2 diabetes mellitus, metabolic syndrome, and insulin resistance. However, the relationship between NAFLD and CKD is poorly understood. We examined the prevalence of and risk factors for CKD in patients with NAFLD. We analyzed 174 Japanese patients with liver biopsy-proven NAFLD using a cross-sectional design. Chronic kidney disease was defined as estimated glomerular filtration rate less than 60 mL/min per 1.73 m(2) and/or overt proteinuria. Of 174 NAFLD patients, 92 (53%) exhibited histologic characteristics of nonalcoholic steatohepatitis (NASH), the progressive form of NAFLD; and 82 (47%) had non-NASH NAFLD. Chronic kidney disease was present in 24 (14%) of 174 NAFLD patients. The prevalence of CKD was significantly higher in NASH patients (19 of 92; 21%) than non-NASH patients (5 of 82; 6%). The presence of CKD was associated with a higher body mass index and the presence of hypertension and NASH. Our results demonstrated a high prevalence of CKD among patients with NASH.
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PMID:Nonalcoholic steatohepatitis and increased risk of chronic kidney disease. 2081 13


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