CMAJ • March 29, 2005; 172 (7). doi:10.1503/cmaj.045232.
© 2005 CMA Media Inc. or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association.
This Article
Right arrow Abstract
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow View Animation
Right arrow Submit a response
Right arrow View responses
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Adams, L. A.
Right arrow Articles by Lindor, K. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Adams, L. A.
Right arrow Articles by Lindor, K. D.
Related Collections
Right arrow Liver (including hepatitis and cirrhosis)

Nonalcoholic fatty liver disease

Leon A. Adams, Paul Angulo and Keith D. Lindor

From the Division of Gastroenterology and Hepatology, Mayo Clinic and College of Medicine, Rochester, Minn.


View this table:

[in a new window]
  		Table 1.

 


View larger version (46K):

[in a new window]
  		Fig. 1: Development of nonalcoholic hepatic steatosis. Insulin resistance enhances triglyceride (TG) lipolysis and inhibits esterification of free fatty acids (FFA) within adipose tissue. The result is increased serum FFA levels, which are taken up by the liver. Hepatic TG synthesis is driven by the increased influx of FFA and favoured by insulin upregulated lipogenic transcription factors, such as peroxisome proliferator-activated receptor gamma (PPAR{gamma}) and sterol regulatory element binding protein (SREBP)-1c. Alternative metabolism of FFA by oxidation is inhibited by insulin. TG export via very-low-density lipoproteins (VLDL) may be inhibited by decreased synthesis of apolipoprotein B (apo B) or reduced incorporation of TG with apo B by microsomal triglyceride transfer protein (MTP). See the animated figure at www.cmaj.ca/cgi/content/full/172/7/899/DC1. Photo: Mayo Clinic

 


View larger version (138K):

[in a new window]
  		Fig. 2: Left: Histologic features of fibrosis in nonalcoholic steatohepatitis (NASH). Trichrome stain of liver (magnification 200) demonstrating macrovesicular steatosis and fibrosis, most prominent in zone 3 near the central vein (CV) of the hepatic lobule. Typically early fibrosis is pericellular and perisinusoidal, giving the appearance of "chickenwire." Right: Histologic features of necrotic inflammation in NASH. Hematoxylin and eosin stain of liver (magnification 400) with injured ballooned hepatocytes (B) and a mild neutrophilic infiltrate (N). Aggregations of Mallory's hyaline (MH) comprised of eosinophilic cytoskeleton filaments are also observed.

 


View larger version (162K):

[in a new window]
  		Figure 2. Continued.

 

View this table:

[in a new window]
  		Table 2.