scholarly journals Peroxisome Proliferator-Activated Receptor Genetic Polymorphisms and Nonalcoholic Fatty Liver Disease: Any Role in Disease Susceptibility?

PPAR Research ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Paola Dongiovanni ◽  
Luca Valenti
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Peroxisome Proliferator ◽  
Nonalcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
The Impact

Nonalcoholic fatty liver disease (NAFLD) defines a wide spectrum of liver diseases that extend from simple steatosis, that is, increased hepatic lipid content, to nonalcoholic steatohepatitis (NASH), a condition that may progress to cirrhosis with its associated complications. Nuclear hormone receptors act as intracellular lipid sensors that coordinate genetic networks regulating lipid metabolism and energy utilization. This family of transcription factors, in particular peroxisome proliferator-activated receptors (PPARs), represents attractive drug targets for the management of NAFLD and NASH, as well as related conditions such as type 2 diabetes and the metabolic syndrome. The impact on the regulation of lipid metabolism observed for PPARs has led to the hypothesis that genetic variants within the human PPARs genes may be associated with human disease such as NAFLD, the metabolic syndrome, and/or coronary heart disease. Here we review the available evidence on the association between PPARs genetic polymorphism and the susceptibility to NAFLD and NASH, and we provide a meta-analysis of the available evidence. The impact of PPAR variants on the susceptibility to NASH in specific subgroup of patients, and in particular on the response to therapies, especially those targeting PPARs, represents promising new areas of investigation.

Nonalcoholic fatty liver disease in patients with hepatitis C is associated with features of the metabolic syndrome

2003 ◽  
Vol 98 (9) ◽  
pp. 2064-2071 ◽  
Author(s):  
Arun J. Sanyal ◽  
Melissa J. Contos ◽  
Richard K. Sterling ◽  
Velimir A. Luketic ◽  
Mitchell L. Shiffman ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Hepatitis C ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
The Metabolic Syndrome

scholarly journals Insulin Resistance, the Metabolic Syndrome, and Nonalcoholic Fatty Liver Disease

2005 ◽  
Vol 90 (3) ◽  
pp. 1578-1582 ◽  
Author(s):  
F. Angelico ◽  
M. Del Ben ◽  
R. Conti ◽  
S. Francioso ◽  
K. Feole ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Oral Glucose ◽  
Nonalcoholic Fatty Liver ◽  
Insulin Resistant ◽  
The Metabolic Syndrome

Background/Aims: An association of nonalcoholic fatty liver disease with the insulin-resistant metabolic syndrome has been suggested. The aim of the study was to assess the association of fatty liver to different degrees of insulin resistance and secretion. Methods and Results: The study was performed in 308 alcohol- and virus-negative consecutive patients attending a metabolic clinic, who underwent a complete clinical and biochemical work-up including oral glucose tolerance test and routine liver ultrasonography. Steatosis was graded as absent/mild, moderate, and severe. In nondiabetic subjects, a progressive (P < 0.05) increase in mean homeostasis model of insulin resistance was recorded from the group without steatosis to the groups with mild/moderate and severe steatosis. Severe steatosis was associated with the clustering of the five clinical and biochemical features proposed for the clinical diagnosis of the metabolic syndrome. Subjects with the metabolic syndrome with a more pronounced insulin resistance had a higher prevalence of severe steatosis (P < 0.01) compared with those with homeostasis model of insulin resistance below the median. Conclusions: The findings stress the heterogeneous presentation of patients with the metabolic syndrome when the diagnosis is based on the broad Adult Treatment Panel III clinical criteria and demonstrate that those who are more insulin resistant have a higher prevalence of severe steatosis.

Nonalcoholic Fatty Liver Disease as a Contributor to Hypercoagulation and Thrombophilia in the Metabolic Syndrome

2009 ◽  
Vol 35 (03) ◽  
pp. 277-287 ◽  
Author(s):  
Giovanni Targher ◽  
Michel Chonchol ◽  
Luca Miele ◽  
Giacomo Zoppini ◽  
Isabella Pichiri ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
The Metabolic Syndrome

scholarly journals The Relationship Between Serum Visfatin, Blood Glucose, Lipid Metabolism and Nonalcoholic Fatty liver Disease in Simple Obese Children

2019 ◽  
Author(s):  
mostafa Ahmed EL Foly ◽  
lubna Anas Fawaz ◽  
Ashraf Mohammed Osman ◽  
Salwa Hussien Swelam ◽  
Noura Elbakry
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Obese Children ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Abstract Abstract Background Non-alcoholic fatty liver disease (NAFLD) ranges from simple steatosis to nonalcoholic steatohepatitis (NASH)leading to fibrosis and potentially cirrhosis, and it is one of the most common causes of liver disease worldwide.NAFLD is associated with other medical conditions suchas metabolic syndrome, obesity, cardiovascular disease and diabetes. Visfatin is an adipocytokine hormone, which exerts an insulin-like effect by binding to the insulin receptor-1, we aim to investigate the correlation between serum Visfatin and both glucose, lipid metabolism and nonalcoholic fatty liver disease in Simple obese children. Methods: This prospective study included 62 children clinically evaluated as obese and 35 apparently healthy children, age and sex matched as controls. Patients were recruited from the emergency department, in-patient wards and out-patient clinics of thepediatric department of EL-Mina University, children's hospital.While controls were collected from healthy school children during day time between September, 2016 and October, 2017. Fasting Visfatin, glucose, hemoglobinA1cand lipid levels were assayed and abdominal ultrasonography was done for detection of NAFLD. Results There was a statistically significant correlation between serum Visfatin level and BMI (p<0.01), cholesterol levels (p< 0.01), triglycerides levels (p< 0.01), LDL levels (p< 0.01), HDL levels (p< 0.01) in both overweight and obese groups. Conclusions: Visfatin plays an important role in regulation of glucose and lipid metabolism, also in inflammation and insulin resistance, suggesting a role in pathogenesis of Non-Alcoholic Fatty Liver Disease (NAFLD). Key words: Non-alcoholic fatty liver disease; metabolic syndrome; Visfatin

scholarly journals Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases: The Heart of the Matter

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Stefan Chiriac ◽  
Carol Stanciu ◽  
Irina Girleanu ◽  
Camelia Cojocariu ◽  
Catalin Sfarti ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Current Evidence ◽  
Nonalcoholic Fatty Liver ◽  
Pathophysiological Mechanisms ◽  
The Metabolic Syndrome

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most frequent cause of liver disease worldwide, comprising a plethora of conditions, ranging from steatosis to end-stage liver disease. Cardiovascular disease (CVD) has been associated with NAFLD and CVD-related events represent the main cause of death in patients with NAFLD, surpassing liver-related mortality. This association is not surprising as NAFLD has been considered a part of the metabolic syndrome and has been related to numerous CVD risk factors, namely, insulin resistance, abdominal obesity, dyslipidemia, hyperuricemia, chronic kidney disease, and type 2 diabetes. Moreover, both NAFLD and CVD present similar pathophysiological mechanisms, such as increased visceral adiposity, altered lipid metabolism, increased oxidative stress, and systemic inflammation that could explain their association. Whether NAFLD increases the risk for CVD or these diagnostic entities represent distinct manifestations of the metabolic syndrome has not yet been clarified. This review focuses on the relation between NAFLD and the spectrum of CVD, considering the pathophysiological mechanisms, risk factors, current evidence, and future directions.

Does Nonalcoholic Fatty Liver Disease Predispose Patients to Hepatocellular Carcinoma in the Absence of Cirrhosis?

2008 ◽  
Vol 132 (11) ◽  
pp. 1761-1766 ◽  
Author(s):  
Grace Guzman ◽  
Elizabeth M. Brunt ◽  
Lydia M. Petrovic ◽  
Gregorio Chejfec ◽  
Thomas J. Layden ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Laboratory Data ◽  
Key Words Hepatocellular Carcinoma ◽  
Nonalcoholic Fatty Liver ◽  
The Metabolic Syndrome

Abstract Context.—Hepatocellular carcinoma (HCC) is recognized as a complication of cirrhosis related to nonalcoholic fatty liver disease (NAFLD). Diabetes and the metabolic syndrome are also associated with HCC. However, it is not clear whether NAFLD predisposes patients to HCC in the absence of cirrhosis. Objective.—To seek evidence that HCC can develop in NAFLD unaccompanied by cirrhosis. Design.—Retrospective case study was performed on cases from 2004 to 2007 at the University of Illinois at Chicago Medical Center, using the key words hepatocellular carcinoma, liver explant, and liver resection. The diagnosis of HCC was identified and confirmed by hematoxylin-eosin–stained slides in 50 cases. Cause of liver disease was determined by review of liver histology, clinical history, and laboratory data. Results.—Three patients presented with advanced HCC with features of metabolic syndrome, including an elevated body mass index. Each patient had bland steatosis on liver biopsy, without fibrosis or cirrhosis. None of the 3 patients had evidence of any cause for liver disease other than NAFLD. Conclusions.—The cases presented here suggest that NAFLD may predispose patients to HCC in the absence of cirrhosis. Further studies are needed to confirm this potentially important observation.

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