الفهرس 
NAFLDOnly 14 pages are availabe for public view
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is the commonest hepatic disease in many parts of the World, with an estimated pooled overall global prevalence of NAFLD diagnosed by imaging of 25.24%. (Younossi et al., 2016)
Following the consensus clinical guideline of the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association, NAFLD was defined as the presence of hepatic steatosis by imaging [ultrasonography (US) or computed tomography scanning (CT)] with no causes for secondary hepatic fat accumulation. (Chalasani et al., 2012)
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathologic conditions ranging from simple steatosis (nonalcoholic fatty liver) to nonalcoholic steatohepatitis (NASH) possibly progressing to cirrhosis and hepatic cancer. The most credited explanation for the growing prevalence of NAFLD is the rise in such insulin-resistance conditions as obesity, the metabolic syndrome, and diabetes. Excess adiposity is associated with increased lipid influx into the liver and de novo hepatic lipogenesis, which promote hepatic triglyceride accumulation. Nonalcoholic fatty liver disease has also been suggested to be an early mediator of atherosclerosis and a major factor in the development and progression of cardiovascular disease, especially in people with type 2 diabetes. Recently, it has been shown that the excessive rate of chronic liver disease in type 2 diabetes is similar to that of cardiovascular complications, suggesting that end-stage liver disease should be added to the list of known complications of diabetes. The prevalence of NAFLD in type 2 diabetes is 66%, double the 20% to 30% in the general population. (Giorda et al., 2017)
Since the prevalence of T2DM has risen dramatically in recent years, NAFLD represents a major potential threat to public health. The clinical management of NAFLD is a challenge that has stimulated a growing research interest. Systematic screening for NAFLD in adults is currently not universally recommended in primary care or among high-risk patients attending diabetes or obesity clinics, in part due to uncertainties surrounding its diagnosis and treatment, but also because a cost-effective screening test for the condition has not been established. Invasive or expensive diagnostic options, such as liver biopsy or imaging tests, should be utilised in the context of available resources, with consideration of the burden on healthcare systems and the limitation of current effective treatments for NAFLD. (European Association for the Study of Obesity, 2016)
Although it is deemed to be of key importance in identifying specific targets for treatment, the pathogenesis of NAFLD remains incompletely understood. Various theories have been put forward over time and it has become increasingly clear that a bidirectional cause-and-effect relationship links NAFLD with those metabolic derangements mechanistically belonging to the domain of metabolic syndrome (MS), such as visceral obesity, arterial hypertension, impaired glucose disposal, insulin resistance (IR), atherogenic dyslipidemia, hyperuricemia and iron overload. (Ballestri et al., 2016 )
Insulin resistance (IR) is defined as a reduced biological response to the actions of insulin, causing the fat, muscle and liver tissues to become unable to metabolize glucose and fatty acids, being exacerbated by obesity and the intake of dietary fats. Thus, the association between IR and deposition of triglycerides in the liver, being evaluated by evaluation model index or the homeostasis model assessment-IR (HOMA-IR) is an important instrument. (Cruz et al., 2015)
The Homeostasis Model Assessment of IR (HOMAIR) has proved to be a robust tool for the assessment of IR and is the index of IR that is most widely used in large population studies. The HOMA of β-cell function and IR was first described in 1985 . HOMA-IR is determined using the following simplified equations:
HOMA-IR = [plasma glucose (mg/dL) × plasma insulin (μU/mL)] / 405. (Qi Tang et al., 2015).