Abstract
Nonalcoholic Fatty Liver Disease (NAFLD), a common cause of chronic liver disease, represents a spectrum of histopathologic abnormalities. NAFLD is often associated to the typical components of the metabolic syndrome (MS), with characteristics including abdominal obesity, type 2 diabetes, Insulin Resistance (IR), hypertension, and Hypertriglyceridemia, and has seriously threatened human health. IR, a crucial element of MS, is the fundamental contributor in the process of NAFLD. Therapy strategies are finite and, for now, are basically concentrated on weight reduction and utilization of insulin sensitizing agents. Recent literature indicated IR related to the abnormal glucose metabolism play a pivotal role in the development of NAFLD. Moreover, glucose resistance, glucocorticoid hormones, leptin, et al are also associated with glucose metabolism dysfunction in NAFLD. We highlight the mechanisms of these components in NAFLD, and our work might be beneficial for comprehending the mechanism and treatment of abnormal glucose metabolism in patients with NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by hepatic steatosis
The multiple-hit hypothesis defines insulin resistance (IR) as a key contributor in the pathogenesis of NAFLD because of its impact on increases in de novo lipogenesis and dysfunction in the release of Free Fatty Acids (FFAs) and triglycerides from the liver, which plays a central role in metabolic syndrome
It is seen that NAFLD was independently associated with impaired glucose metabolism [2]
Summary
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by hepatic steatosis. The multiple-hit hypothesis defines insulin resistance (IR) as a key contributor in the pathogenesis of NAFLD because of its impact on increases in de novo lipogenesis and dysfunction in the release of Free Fatty Acids (FFAs) and triglycerides from the liver, which plays a central role in metabolic syndrome (e.g., obesity, type 2 diabetes mellitus, dyslipidemia, hypertension). The role of IR on the progression of NAFLD has not been fully defined. Recent studies show that a NAFLD patient with type 2 diabetes mellitus prevalence rate was 30%-50% [1]. A study described that the prevalence of NAFLD increased with increasing fasting plasma glucose levels. It is seen that NAFLD was independently associated with impaired glucose metabolism [2]
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