1. NAFLD, Obesity, and Bariatric Surgery
Paul Angulo 
Gastroenterology 
Volume 130, Issue 6, Pages (May 2006)
DOI: /j.gastro
Copyright © 2006 American Gastroenterological Association Institute Terms and Conditions

2. Figure 1
The most abundant cellular element in adipose tissue of lean subjects is mature adipocytes. Less numerous are stromal cells including isolated macrophages, lymphocytes, and preadipocytes (ie, immature adipocytes). Obesity alters both the cellular composition and function of adipose tissue. Adipose tissue of obese individuals contains an increased number of macrophages, which seem to originate mostly from the bone marrow and possibly also from transdifferentiation of preadipocytes. Macrophages, endothelial cells, and to a lesser degree, adipocytes, and other cellular components of adipose tissue produce numerous circulating inflammatory markers including pro- and anti-inflammatory factors, chemokines, growth factors, and proteases that induce a systemic low-grade inflammatory state and insulin resistance. This obesity-induced chronic inflammatory state and insulin resistance seen in individuals with increased body mass index, and in particular in those with increased visceral adipose tissue, has a systemic effect inducing several metabolic complications and increased cardiovascular risk profile. The liver component of this metabolic disarray is NAFLD, which includes a spectrum of liver pathology ranging from bland steatosis to cirrhosis, with steatohepatitis being an intermediate stage between those 2 extreme lesions. Successful lifestyle intervention, antiobesity medications, and bariatric surgery induce weight loss and decrease in the amount of visceral fat. Weight loss achieved by these antiobesity modalities is accompanied by normalization of the several inflammatory mediator levels and improvement or resolution of insulin resistance and the obesity-related metabolic complications. Abbreviations: TNF-α, tumor necrosis factor α; IL-6, interleukin 6; IL-1, interleukin 1; TGF-β, transforming growth factor β; MCP, monocyte chemoattractant protein 1; FFA, free fatty acids; CRP, C-reactive protein; VEGF, vascular endothelial growth factor; PAI-1, plasminogen activator inhibitor 1. Steatosis, hematoxylin-eosin stain, magnification 100×. Steatohepatitis, hematoxylin-eosin stain, magnification 100×. Fibrosis, trichrome stain, magnification 400×. Cirrhosis, trichrome stain, magnification 100×. Illustration by Jerry Schoendorf, MAMS.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Institute Terms and Conditions