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Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:4-7
doi: 10.1161/01.ATV.0000253905.13219.4b
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:4.)
© 2007 American Heart Association, Inc.


Editorials

Gamma-Glutamyl Transferase

Another Biomarker for Metabolic Syndrome and Cardiovascular Risk

Scott M. Grundy

From the Center for Human Nutrition and Departments of Clinical Nutrition and Internal Medicine, University of Texas Southwestern Medical Center at Dallas.

Correspondence to Scott M. Grundy, Center for Human Nutrition and Departments of Clinical Nutrition and Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Y3.206, Dallas, TX 75390-9052. E-mail scott.grundy@utsouthwestern.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Gamma-glutamyl transferase (GGT) is a cell-surface protein contributing to the extracellular catabolism of glutathione (GSH).1 The enzyme is produced in many tissues, but most GGT in serum is derived from the liver.1 In the serum, GGT is carried primarily with lipoproteins and albumin.2 Serum levels of GGT are determined by several factors: alcohol intake, body fat content, plasma lipid/lipoproteins and glucose levels, and various medications.1,3,4

See page 127

High levels of GGT have been associated in populations with increased risk of atherosclerotic cardiovascular disease (CVD).5,6 In the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Lee et al7 report that in 3451 Framingham Study participants (mean age 44 years, 52% women) an increased serum GGT predicted the onset of metabolic syndrome and the occurrence of CVD and death; moreover, the highest GGT quartile experienced a 67% increase in CVD incidence. In this study the association of GGT concentrations with CVD and mortality remained significant after adjustment for traditional cardiac risk factors and C-reactive protein (CRP).

One hypothesis for the relation of GGT levels and CVD holds that GGT itself is proatherogenic.1 GGT has been reported to occur in atherosclerotic plaques,8 which might support this hypothesis. The origins of GGT in plaques could be through influx of lipoproteins that carry it into lesions. One of the products of GSH hydrolysis produced by GGT is cyseinyl-glyceine, which can generate superoxidide anion radicals through its interaction with free iron.9 This effect could promote atherogenesis via LDL oxidation. At present the postulated pathogenic . . . [Full Text of this Article]


Related Article:

Gamma Glutamyl Transferase and Metabolic Syndrome, Cardiovascular Disease, and Mortality Risk: The Framingham Heart Study
Douglas S. Lee, Jane C. Evans, Sander J. Robins, Peter W. Wilson, Irene Albano, Caroline S. Fox, Thomas J. Wang, Emelia J. Benjamin, Ralph B. D’Agostino, and Ramachandran S. Vasan
Arterioscler Thromb Vasc Biol 2007 27: 127-133. [Abstract] [Full Text] [PDF]



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Is Serum Gamma-Glutamyltransferase a Biomarker of Xenobiotics, Which Are Conjugated by Glutathione?
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