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World J Gastroenterol. Jul 28, 2014; 20(28): 9330-9337
Published online Jul 28, 2014. doi: 10.3748/wjg.v20.i28.9330
Non-alcoholic fatty liver disease and obesity: Biochemical, metabolic and clinical presentations
Sandra Milić, Davorka Lulić, Davor Štimac
Sandra Milić, Davorka Lulić, Davor Štimac, Division of Gastroenterology, Department of Internal Medicine, University Hospital Rijeka, Rijeka 51000, Croatia
Author contributions: Milić S, Lulić D and Štimac D performed data acquisition and wrote the manuscript; Milić S revised the manuscript; Štimac D approved the final manuscript version.
Correspondence to: Sandra Milić, MD, PhD, Professor, Division of Gastroenterology, Department of Internal Medicine, University Hospital Rijeka, Krešimirova 42, Rijeka 51000, Croatia. smilic05@gmail.com
Telephone: +385-51-658122 Fax: +385-51-658826
Received: October 29, 2013
Revised: January 26, 2014
Accepted: March 19, 2014
Published online: July 28, 2014
Processing time: 270 Days and 8.3 Hours
Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Presentation of the disease ranges from simple steatosis to non-alcoholic steatohepatitis (NASH). NAFLD is a hepatic manifestation of metabolic syndrome that includes central abdominal obesity along with other components. Up to 80% of patients with NAFLD are obese, defined as a body mass index (BMI) > 30 kg/m2. However, the distribution of fat tissue plays a greater role in insulin resistance than the BMI. The large amount of visceral adipose tissue (VAT) in morbidly obese (BMI > 40 kg/m2) individuals contributes to a high prevalence of NAFLD. Free fatty acids derived from VAT tissue, as well as from dietary sources and de novo lipogenesis, are released to the portal venous system. Excess free fatty acids and chronic low-grade inflammation from VAT are considered to be two of the most important factors contributing to liver injury progression in NAFLD. In addition, secretion of adipokines from VAT as well as lipid accumulation in the liver further promotes inflammation through nuclear factor kappa B signaling pathways, which are also activated by free fatty acids, and contribute to insulin resistance. Most NAFLD patients are asymptomatic on clinical presentation, even though some may present with fatigue, dyspepsia, dull pain in the liver and hepatosplenomegaly. Treatment for NAFLD and NASH involves weight reduction through lifestyle modifications, anti-obesity medication and bariatric surgery. This article reviews the available information on the biochemical and metabolic phenotypes associated with obesity and fatty liver disease. The relative contribution of visceral and liver fat to insulin resistance is discussed, and recommendations for clinical evaluation of affected individuals is provided.

Keywords: Fatty liver; Insulin resistance; Intra-abdominal fat; Metabolism; Non-alcoholic fatty liver disease; Obesity

Core tip: This article reviews biochemical, metabolic and clinical relationships between non-alcoholic fatty liver disease and obesity. Visceral adipose tissue influences hepatic steatosis to a greater extent than the body mass index, despite evidence that liver fat may develop independent of skeletal muscle and adipose tissue insulin resistance. Obese individuals with non-alcoholic fatty liver disease usually present with symptoms of metabolic syndrome or its components.