Molecular mechanisms involved in NAFLD progression

Abstract

Non-alcoholic fatty liver disease (NAFLD) is an emerging metabolic-related disorder characterized by fatty infiltration of the liver in the absence of alcohol consumption. NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), which might progress to end-stage liver disease. This progression is related to the insulin resistance, which is strongly linked to the metabolic syndrome consisting of central obesity, diabetes mellitus, and hypertension. Earlier, the increased concentration of intracellular fatty acids within hepatocytes leads to steatosis. Subsequently, multifactorial complex interactions between nutritional factors, lifestyle, and genetic determinants promote necrosis, inflammation, fibrosis, and hepatocellular damage. Up to now, many studies have revealed the mechanism associated with insulin resistance, whereas the mechanisms related to the molecular components have been incompletely characterized. This review aims to assess the potential molecular mediators initiating and supporting the progression of NASH to establish precocious diagnosis and to plan more specific treatment for this disease.

Porphyromonas gingivalis induced periodontitis exacerbates progression of non‐alcoholic steatohepatitis in rats

“…It has been reported that various factors are associated with the pathogenesis of NASH, including oxidative stress, insulin resistance, and adipocytokines (Sanyal, 2011; Malaguarnera, Rosa, Nicoletti, & Malaguarnera, 2009). However, it is unclear whether other factors are related to the onset and progression of NASH.…”

Anti–oxidative role of quercetin derived from Allium cepa on aldehyde oxidase (OX–LDL) and hepatocytes apoptosis in streptozotocin–induced diabetic rat

“…Investigations show liver has an important role in carbohydrate metabolism since it is responsible for the balance of blood glucose level by means of glycogen sis and glycogenolysis therefore impaired hepatic function impairs metabolic homeostasis of glucose [1,16] . In the presence of impaired glucose metabolism and occurrence of hyperglycemia, genes involved in fatty acid storage were activated [17] . On the other hand, liver diseases can induce diabetes mellitus.…”

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 first hit initiates LS, and the second hit stimulates inflammatory processes. These two conditions may result in hepatocyte injury and fibrosis [4,5]. NAFLD is asymptomatic, undetectable, and progressive.…”

“…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.…”