Abstract
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of clinicopathologic conditions ranging from steatosis alone to nonalcoholic steatohepatitis (NASH), with varying risks for progression to cirrhosis and hepatocellular carcinoma. There is mounting evidence that NAFLD not only complicates obesity, but also perpetuates its metabolic consequences. Critical event that leads to progressive liver injury in NAFLD is unknown. Obesity reflects a generalized proinflammatory state with its increased inflammatory markers like C reactive protein, IL-6, IL-8, IL-10, PAI-1, TNF-α, and hepatocyte growth factor. The elevated production of these adipokines is increasingly considered to be important in the development of diseases linked to obesity and the metabolic syndrome. Disordered cytokine production is likely to play a role in the pathogenesis of NAFLD. There is no effective treatment for NAFLD, though weight loss may halt disease progression and revert histological changes, the underlying mechanism remaining elusive. All stages of the disease pathway from prevention, early identification/diagnosis, and treatment require an understanding of the pathogenesis of liver injury in NAFLD.
Highlights
With the rapidly growing prevalence of obesity [1] throughout the world, morbidity and mortality related to its complications is on the rise [2]
It is clear that patients with Nonalcoholic fatty liver disease (NAFLD) and even more so with nonalcoholic steatohepatitis (NASH) have a serious liver disease with a fibrogenic potential that can result in liver-related morbidity and mortality
Compared to Caucasians, lower levels of hepatic triglycerides have been found in African Americans despite similar total body adiposity and insulin resistance [166, 168], whilst Asians have increased visceral fat depots in relation to their body mass index (BMI) risking NAFLD despite low BMI [166, 169]
Summary
With the rapidly growing prevalence of obesity [1] throughout the world, morbidity and mortality related to its complications is on the rise [2]. NAFLD represents the most common of all liver disorders and the most frequent cause of chronic liver disease [7]. It is a syndrome with multifactorial aetiology with which obesity is most commonly associated [8]. Obesity itself is typically a heterogeneous condition due to the regional distribution of fat tissue. There is growing evidence that the distribution of adipose tissue in the body is of importance for the development of the metabolic complications of obesity. Adipose tissue as an endocrine organ has become accepted [9, 10] with the distinctive biological properties of visceral adipose tissue presumably contributing to the increased pathogenecity of obesity
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