Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome

Abstract

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.

Houttuynia cordataalleviates high-fat diet-induced non-alcoholic fatty liver in experimental rats

“…Hypercholesterolemia, hypertriglyceridemia, low HDL-C levels, and high LDL-C levels are the most common impairments in lipid homeostasis in patients with hepatic steatosis (Moore, 2010). In our model, HFD-fed rats developed hepatic steatosis, visceral obesity, hyperlipidemia, and increased FFA, which mimics almost all the clinical aspects of human NAFLD (Xu et al, 2010).…”

Downregulation of Sulfotransferase Expression and Activity in Diseased Human Livers

“…NAFLD is the most common chronic liver disease in the industrialized countries. Current estimates of NAFLD range from 5% to 33% of United States population, but true prevalence is likely to be higher as many people remain undiagnosed in early stages due to the lack of inexpensive and noninvasive screening tests (Lazo and Clark, 2008;Moore, 2010). NAFLD is characterized as the accumulation of fat in liver in the absence of excessive alcohol intake.…”

Supplementation With 2:1 Ratio of N-6:n-3 Polyunsaturated Fatty Acid Improves Liver Steatosis and Serum Cytokine Levels in Young Obese Balinese Women: A Randomized Clinical Trial

“…NAFLD is the most common liver disorder and is the leading cause of hepatocyte injury and fibrosis. NAFLD is also associated with chronic liver diseases such as cirrhosis [4][5][6][7][8].…”

“…The prevalence of LS is higher among patients with obesity and type 2 diabetes (70-80%), and as many as 25-70% of these patients eventually develop chronic liver diseases such as NASH and fibrosis [6][7][8]. Obesity, a high-fat diet, a genetic predisposition, and microbiota have been identified as risk factors for NAFL [4][5][6][7][8]. In obese patients associated chronic inflammatory states, the adipose tissue releases more pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, whereas the release of IL-10 is decreased.…”

“…In obese patients associated chronic inflammatory states, the adipose tissue releases more pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, whereas the release of IL-10 is decreased. Moreover, the levels of pro-inflammatory cytokines, such as TNF-α and IL-16, produced by the liver and adipose tissue are elevated during the activation of nuclear factor kappa B. TNF-α involves in inflammatory and metabolic alterations nearly stage of liver injury, leading to increased cytokines synthesis, which in turn induces cell migration, initiate fibrotic processes, and influence the progression of NAFL to NASH [4][5][6][7][8]. By contrast, IL-10 inhibits the synthesis of pro-inflammatory cytokines such as interferon-γ, IL-2, IL-3, and TNF-α.…”