Obesity, smoking and fatty liver disease

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Background

Approximately 20% (~60 million) of Americans smoke and about ~88 million nonsmokers were exposed to secondhand smoke. Cigarette smoking (CS) is a major cause of premature death worldwide. CS constitutes a major risk factor for cardiovascular disease, chronic obstructive pulmonary disease, lung cancers, type 2 diabetes mellitus (DM) and more recently nonalcoholic fatty liver disease (NAFLD). NAFLD is the most common of liver pathologies associated with metabolic syndrome and DM. It includes the whole spectrum of fatty liver, ranging from simple steatosis to steatohepatitis (NASH), which can progress to liver cirrhosis and hepatocellular carcinoma. Of note, usages of nicotine-only formulations such as transdermal patches, nicotine gum, and electronic cigarettes, in particular, are increasing.

The health risk associated with smoking is exaggerated by obesity, and smoking and obesity are the leading causes of morbidity and mortality worldwide. The life expectancy of an obese smoker was 13 y less than that of normal weight nonsmoker. Currently, 34% of the general population and over 75% of the obese and extremely obese individuals are estimated to have fatty liver. Given that obesity is epidemic and that smoking prevalence or nicotine use is high and on the rise in many developing countries, it is clear that the co-occurrence of the two increases with devastating effects on overall heath throughout the world.

The presence of steatosis is associated with a constellation of adverse alterations in glucose, fatty acid, and lipoprotein metabolism. Intrahepatic triglyceride content was associated with progressive impairment of insulin action in liver, skeletal muscle, and adipose tissue in nondiabetic obese subjects and thus NAFLD should be considered part of a multi-organ system derangement in insulin sensitivity. Oxidative stress coupled with hepatocyte apoptosis is believed to play a pivotal role in pathogenesis of NAFLD. In fact, emerging data suggest that hepatocellular apoptosis plays a key component in the progression of simple steatosis to NASH. Emerging evidence now suggests that CS or nicotine exacerbates hepatic steatosis triggered by high-fat diet, through increased oxidative stress and hepatocellular apoptosis, decreased phosphorylation (inactivation) of adenosine-5-monophosphate-activated protein kinase and, in turn, up-regulation of sterol response-element binding protein 1-c, fatty acid synthase, and activation acetyl-COA-carboxylase leading to increased hepatic lipogenesis.

In this research topic, we will provide a comprehensive assessment of the impact of smoking and obesity on metabolic homeostasis, insulin resistance, and address recent advances in molecular underpinning of fatty liver disease.

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