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Diabetes Care 31:e43 2008
DOI: 10.2337/dc08-0223
© 2008 by the American Diabetes Association
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Online Letters: Comments and Responses

Should Nonalcoholic Fatty Liver Disease Be Included in the Definition of Metabolic Syndrome? A Cross-Sectional Comparison With Adult Treatment Panel III Criteria in Nonobese Nondiabetic Subjects

Response to Sookoian et al.

Giovanni Musso, MD1, Roberto Gambino, MD2, Simona Bo, MD2 and Maurizio Cassader, MD2

1 Gradenigo Hospital, Turin, Italy
2 Department of Internal Medicine, University of Turin, Turin, Italy

Corresponding author: Giovanni Musso, Gradenigo Hospital, Corso R. Margherita 8, 10132 Torino, Italy. E-mail: giovanni_musso{at}yahoo.it

The findings of Sookoian et al. (1) expand our recent research (2) and further suggest that the liver, the vessel wall, and adipose tissue share common inflammatory pathways. Intracellular adhesion molecule-1 (ICAM-1) is a transmembrane adhesion molecule involved in leukocyte migration to inflammatory sites, and soluble ICAM-1 levels have been associated with endothelial dysfunction and early atherosclerosis in the general population.

Innate immune response cells, including natural killer and Kupffer cells, are more common in the liver than in peripheral blood or other organs like the spleen; these cells play a key role in different animal and human models of liver injury, including endotoxin-, alcohol-, and viral hepatitis–induced injury (3,4). Recently, a pathogenetic role for endotoxin-induced liver injury has also been proposed for NAFLD (5).

Increased sinusoidal endothelial ICAM-1 expression was found to play an important role in innate immune cell recruitment and local cytokine production in the liver (5); furthermore, dietary factors, like a high-fat diet, enhanced adipose tissue ICAM-1 expression, and subsequent immune cell infiltration, inducing a local and systemic proinflammatory state in animal models (6). Altogether, these findings suggest that circulating ICAM-1 levels may be potentially useful not only for noninvasive assessment of liver injury in NAFLD but also for evaluating overall inflammatory balance and cardiometabolic risk in obesity-related metabolic disorders.

References

  1. Sookoian S, Burgueño AL, Castaño G, Pirola CJ. Should nonalcoholic fatty liver disease be included in the definition of metabolic syndrome? A cross-sectional comparison with Adult Treatment Panel III criteria in nonobese nondiabetic subjects (Letter). Diabetes Care 31:e42, 2008. DOI:10.2337/dc08-0027[Free Full Text]
  2. Musso G, Gambino R, Bo S, Uberti B, Broli G, Pagano G, Cassader M: Should nonalcoholic fatty liver disease be included in the definition of metabolic syndrome? A cross-sectional comparison with Adult Treatment Panel III criteria in nonobese nondiabetic subjects. Diabetes Care 31:562–568, 2008[Abstract/Free Full Text]
  3. Dong Z, Wei H, Sun R, Tian Z: The roles of innate immune cells in liver injury and regeneration. Cell Mol Immun 4:241–252, 2007
  4. Ohira H, Abe K, Yokokawa J, Takiguchi J, Rai T, Shishido S, Sato Y: Adhesion molecules and CXC chemokines in endotoxin-induced liver injury. Fukushima J Med Sci 49:1–13, 2003[Medline]
  5. Ma X, Hua J, Mohamood AR, Hamad AR, Ravi R, Li Z: High-fat diet and regulatory T cells influence susceptibility to endotoxin-induced liver injury. Hepatology 46:1519–29, 2007[Medline]
  6. Brake DK, Smith EO, Mersmann H, Smith CW, Robker RL: ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice. Am J Physiol Cell Physiol 291:C1232–C1239, 2006[Abstract/Free Full Text]

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This Article
Right arrow Extract Freely available
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Right arrow Purchase Article
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Google Scholar
Right arrow Articles by Musso, G.
Right arrow Articles by Cassader, M.
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Right arrow Articles by Musso, G.
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