doi: 10.1161/01.ATV.0000253905.13219.4b
© 2007 American Heart Association, Inc.
Editorials |
Gamma-Glutamyl Transferase
Another Biomarker for Metabolic Syndrome and Cardiovascular Risk
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{at}utsouthwestern.edu
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 pathways remain hypothetical and are yet to be substantiated.
An alternative hypothesis that appears to be consistent with the findings of Lee et al7 is that elevations of GGT are a marker of the presence of the metabolic syndrome. Other workers have reported that high levels of GGT are associated with fatty liver, insulin resistance, type 2 diabetes, obesity, and other metabolic risk factors. There is growing evidence that the liver, which is the primary source of circulating GGT, is a key target organ for the development of the metabolic syndrome. An elevation of GGT is seemingly closely related to hepatic steatosis10–13; the latter in turn is strongly associated with the metabolic syndrome.14–18 The mechanisms whereby elevated GGT is related to hepatic steatosis have not been determined, but several possibilities have been proposed by Ortega et al.19 For example, fatty liver could cause hepatocellular damage that would simulate the synthesis of GGT. Alternatively, excess fat in the liver could enhance oxidative stress, leading to overconsumption of GSH with a compensatory increase in GGT synthesis. Finally, a higher GGT production could be secondary to a low grade hepatic inflammation induced by hepatic steatosis.
It must be noted that high levels of GGT are not the only hepatic biomarker of hepatic steatosis. Elevations of transaminase are common in patients with fatty liver with or without histological evidence of inflammation.20–24 In addition, higher levels of serum transaminases in populations have been associated with the metabolic syndrome25–30 and a higher risk for CVD.31,32
Other lines of evidence support a relationship between elevated serum GGT and the metabolic syndrome.33 Thus the higher GGT levels are accompanied by more insulin resistance and greater risk for developing type 2 diabetes.34–38 Another important association between GGT and the metabolic syndrome is the finding that higher GGT levels occur in obese persons, particularly those with abdominal obesity.39–44 The connection between GGT and the metabolic syndrome extends to an association of higher GGT levels with hypertension.45–49 Thus, it appears that all of the major components of the metabolic syndrome are linked to elevations of serum GGT.
The metabolic syndrome consists primarily of a group of atherogenic factors that commonly cluster in individuals.50 These include elevations of remnant lipoproteins, glucose, blood pressure, circulating inflammatory cytokines, and prothrombotic factors and low levels of high density lipoproteins (HDL) (Table). In addition, a large number of biomarkers have been reported to be associated with the metabolic syndrome (Table). These include parameters of obesity and products released by adipose tissue, plasma insulin levels and insulin-like growth factors, liver enzymes, C-reactive protein and circulating metabolites, several components of circulating lipoproteins, microalbuminuria, and markers of increased cellular inflammation.51–66 The status of these biomarkers as causative factors, either in generation of the metabolic syndrome or directly in atherogenesis, at present is uncertain. Some of them have been implicated as causes, but others as a reflection of a metabolic abnormality.
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Certainly elevations of serum GGT belong on the list of biomarkers linked to the metabolic syndrome. It appears to be largely a reflection of ectopic liver fat or secondary hepatic inflammation. Although high levels of GGT have been postulated to be directly atherogenic,1 as have several other biomarkers for the metabolic syndrome, a direct role in causation of atherosclerosis remains to be determined. Nonetheless, it is clear that the pathways whereby various biomarkers are connected to the causation and complications of the metabolic syndrome represent a rich field for future research.
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Acknowledgments |
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Disclosures
None.
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References |
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 Top References |
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1. Emdin M, Pompella A, Paolicchi A. Gamma-glutamyltransferase, atherosclerosis, and cardiovascular disease: triggering oxidative stress within the plaque. Circulation. 2005; 112: 2078–2080.
2. Whitfield JB. Gamma-glutamyl transferase. Crit Rev Clin Lab Sci. 2001; 38: 263–3553.[CrossRef][Medline] [Order article via Infotrieve]
3. Brenner H, Rothenbacher D, Arndt V, Schuberth S, Fraisse E, Fliedner TM. Distribution, determinants, and prognostic value of gamma-glutamyltranspeptidase for all-cause mortality in a cohort of construction workers from south Germany. Prev Med. 1997; 26: 305–310.[CrossRef][Medline] [Order article via Infotrieve]
4. Nilssen O, Forde OH, Brenn T. The Tromso Study. Distribution and population determinants of gamma-glutamyltransferase. Am J Epidemiol. 1990; 132: 318–326.
5. Ruttmann E, Brant LJ, Concin H, Diem G, Rapp K, Ulmer H; Vorarlberg Health Monitoring and Promotion Program Study Group. Gamma-glutamyltransferase as a risk factor for cardiovascular disease mortality: an epidemiological investigation in a cohort of 163,944 Austrian adults. Circulation. 2005; 112: 2130–2137.
6. Wannamethee SG, Shaper AG, Lennon L, Whincup PH. Hepatic enzymes, the metabolic syndrome, and the risk of type 2 diabetes in older men. Diabetes Care. 2005; 28: 2913–2918.
7. Lee DS, Evans JC, Robins SJ, Wilson PW, Albano I, Fox CS, Wang TJ, Benjamin EJ, D’Agostino RB, Vasan RS. Gamma glutamyl transferase and metabolic syndrome, cardiovascular disease, and mortality risk: the Framingham Heart Study. Arterioscler Thromb Vasc Biol. 2007; 27: 127–133.
8. Paolicchi A, Emdin M, Ghliozeni E, Ciancia E, Passino C, Popoff G, Pompella A. Human atherosclerotic plaques contain gamma-glutamyl transpeptidase enzyme activity. Circulation. 2004; 109: 1440.
9. Pompella A, Emdin M, Passino C, Paolicchi A. The significance of serum -glutamyltransferase in cardiovascular diseases. Clin Chem Lab Med. 2004; 42: 1085–1091.[CrossRef][Medline] [Order article via Infotrieve]
10. Ludtke A, Genschel J, Brabant G, Bauditz J, Taupitz M, Koch M, Wermke W, Worman HJ, Schmidt HH. Hepatic steatosis in Dunnigan-type familial partial lipodystrophy. Am J Gastroenterol. 2005; 100: 2218–2224.[CrossRef][Medline] [Order article via Infotrieve]
11. Angulo P. Nonalcoholic fatty liver disease. N Engl J Med. 2002; 346: 1221–1231.
12. Neuschwander-Tetri BA, Caldwell SH. Nonalcoholic steatohepatitis: summary of an AASLD Single Topic Conference. Hepatology. 2003; 37: 1202–1219.[CrossRef][Medline] [Order article via Infotrieve]
13. Loguercio C, De Simone T, D’Auria MV, de Sio I, Federico A, Tuccillo C, Abbatecola AM, Del Vecchio Blanco C; Italian AISF Clinical Group. Non-alcoholic fatty liver disease: a multicentre clinical study by the Italian Association for the Study of the Liver. Dig Liver Dis. 2004; 36: 398–405.[Medline] [Order article via Infotrieve]
14. Collantes RS, Ong JP, Younossi ZM. The metabolic syndrome and nonalcoholic fatty liver disease. Panminerva Med. 2006; 48: 41–48.[Medline] [Order article via Infotrieve]
15. The Metabolic Syndrome as a Predictor of Nonalcoholic Fatty Liver Disease M. Hamaguchi, T. Kojima, N. Takeda, T. Nakagawa, H. Taniguchi, K. Fujii, T. Omatsu, T. Nakajima, H. Sarui, M. Shimazaki, T. Kato, J. Okuda and K. Ida. Ann Intern Med. 2005; 143: 722–728.
16. Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, Grundy SM, Hobbs HH. Related Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity. Hepatology. 2004; 40: 1387–1395.[CrossRef][Medline] [Order article via Infotrieve]
17. Yki-Jarvinen H. Ectopic fat accumulation: an important cause of insulin resistance in humans. J R Soc Med. 2002; 95 (Suppl 42): 39–45.
18. Ekstedt M, Franzen LE, Mathiesen UL, Thorelius L, Holmqvist M, Bodemar G, Kechagias S. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology. 2006; 44: 865–873.[CrossRef][Medline] [Order article via Infotrieve]
19. Ortega E, Koska J, Salbe AD, Tataranni PA, Bunt JC. Related Articles, Links Serum gamma-glutamyl transpeptidase is a determinant of insulin resistance independently of adiposity in Pima Indian children. J Clin Endocrinol Metab. 2006; 91: 1419–1422.
20. Loguercio C, De Simone T, D’Auria MV, de Sio I, Federico A, Tuccillo C, Abbatecola AM, Del Vecchio Blanco C; Italian AISF Clinical Group. Non-alcoholic fatty liver disease: a multicentre clinical study by the Italian Association for the Study of the Liver. Dig Liver Dis. 2004; 36: 398–405.[Medline] [Order article via Infotrieve]
21. Clark JM, Brancati FL, Diehl AM. The prevalence and etiology of elevated aminotransferase levels in the United States. Am J Gastroenterol. 2003; 98: 960–967.[CrossRef][Medline] [Order article via Infotrieve]
22. Fishbein MH, Miner M, Mogren C, Chalekson J. The spectrum of fatty liver in obese children and the relationship of serum aminotransferases to severity of steatosis. J Pediatr Gastroenterol Nutr. 2003; 36: 54–61.[CrossRef][Medline] [Order article via Infotrieve]
23. Daniel S, Ben-Menachem T, Vasudevan G, Ma CK, Blumenkehl M. Prospective evaluation of unexplained chronic liver transaminase abnormalities in asymptomatic and symptomatic patients. Am J Gastroenterol. 1999; 94: 3010–3014.[CrossRef][Medline] [Order article via Infotrieve]
24. Sorbi D, Boynton J, Lindor KD. The ratio of aspartate aminotransferase to alanine aminotransferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver disease. Am J Gastroenterol. 1999; 94: 1018–1022.[CrossRef][Medline] [Order article via Infotrieve]
25. Su CC, Wang K, Hsia TL, Chen CS, Tung TH. Association of nonalcoholic fatty liver disease with abnormal aminotransferase and postprandial hyperglycemia. J Clin Gastroenterol. 2006; 40: 551–554.[CrossRef][Medline] [Order article via Infotrieve]
26. Kazumi T, Kawaguchi A, Hirano T, Yoshino G. Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. Horm Metab Res. 2006; 38: 119–124.[CrossRef][Medline] [Order article via Infotrieve]
27. Kazumi T, Kawaguchi A, Hirano T, Yoshino G. Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. Horm Metab Res. 2006; 38: 119–124.[CrossRef][Medline] [Order article via Infotrieve]
28. Onat A, Hergenc G, Karabulut A, Turkmen S, Dogan Y, Uyarel H, Can G, Sansoy V. Serum gamma glutamyltransferase as a marker of metabolic syndrome and coronary disease likelihood in nondiabetic middle-aged and elderly adults. Prev Med. 2006; 43: 136–139.[CrossRef][Medline] [Order article via Infotrieve]
29. Choi KM, Lee KW, Kim HY, Seo JA, Kim SG, Kim NH, Choi DS, Baik SH. Association among serum ferritin, alanine aminotransferase levels, and metabolic syndrome in Korean postmenopausal women. Metabolism. 2005; 54: 1510–1514.[CrossRef][Medline] [Order article via Infotrieve]
30. Hanley AJ, Williams K, Festa A, Wagenknecht LE, D’Agostino RB Jr, Haffner SM. Liver markers and development of the metabolic syndrome: the insulin resistance atherosclerosis study. Diabetes. 2005; 54: 3140–3147.
31. Bouter LM, Stehouwer CD, Heine RJ, Diamant M. Alanine aminotransferase predicts coronary heart disease events: A 10-year follow-up of the Hoorn Study. Atherosclerosis. In press.
32. Ioannou GN, Weiss NS, Boyko EJ, Mozaffarian D, Lee SP. Elevated serum alanine aminotransferase activity and calculated risk of coronary heart disease in the United States. Hepatology. 2006; 43: 1145–1151.[CrossRef][Medline] [Order article via Infotrieve]
33. Rantala AO, Lilja M, Kauma H, Savolainen MJ, Reunanen A, Kesaniemi YA. Gamma-glutamyl transpeptidase and the metabolic syndrome. J Intern Med. 2000; 248: 230–238.[CrossRef][Medline] [Order article via Infotrieve]
34. Andre P, Balkau B, Born C, Charles MA, Eschwege E; D.E.S.I.R. study group. Three-year increase of gamma-glutamyltransferase level and development of type 2.diabetes in middle-aged men and women: the D.E.S.I.R. cohort. Diabetologia. 2006; 49: 2599–2603.[CrossRef][Medline] [Order article via Infotrieve]
35. Marchesini G, Avagnina S, Barantani EG, Ciccarone AM, Corica F, Dall’Aglio E, Dalle Grave R, Morpurgo PS, Tomasi F, Vitacolonna E. Aminotransferase and gamma-glutamyltranspeptidase levels in obesity are associated with insulin resistance and the metabolic syndrome. J Endocrinol Invest. 2005; 28: 333–339.[Medline] [Order article via Infotrieve]
36. Thamer C, Tschritter O, Haap M, Shirkavand F, Machann J, Fritsche A, Schick F, Haring H, Stumvoll M. Elevated serum GGT concentrations predict reduced insulin sensitivity and increased intrahepatic lipids. Horm Metab Res. 2005; 37: 246–251.[CrossRef][Medline] [Order article via Infotrieve]
37. Lee DH, Silventoinen K, Jacobs DR Jr, Jousilahti P, Tuomileto J. gamma-Glutamyltransferase, obesity, and the risk of type 2 diabetes: observational cohort study among 20,158 middle-aged men and women. J Clin Endocrinol Metab. 2004; 89: 5410–5414.
38. Nakanishi N, Nishina K, Li W, Sato M, Suzuki K, Tatara K. Serum gamma-glutamyltransferase and development of impaired fasting glucose or type 2 diabetes in middle-aged Japanese men. J Intern Med. 2003; 254: 287–295.[CrossRef][Medline] [Order article via Infotrieve]
39. Lawlor DA, Sattar N, Smith GD, Ebrahim S. The associations of physical activity and adiposity with alanine aminotransferase and gamma-glutamyltransferase. Am J Epidemiol. 2005; 161: 1081–1088.
40. Li TC, Liu CS, Lin CC. The relationship of liver enzyme abnormalities and obesity in Aboriginal children in Taiwan. J Gastroenterol. 2004; 39: 1170–1174.[CrossRef][Medline] [Order article via Infotrieve]
41. Choi JW. Association between elevated serum hepatic enzyme activity and total body fat in obese humans. Ann Clin Lab Sci. 2003; 33: 257–264.
42. Nakanishi N, Nakamura K, Suzuki K, Tatara K. Lifestyle and serum gamma-glutamyltransferase: a study of middle-aged Japanese men. Occup Med (Lond). 2000; 50: 115–120.[Medline] [Order article via Infotrieve]
43. Ikai E, Noborizaka Y, Tsuritani I, Honda R, Ishizaki M, Yamada Y. Serum gamma-glutamyl transpeptidase levels and hypertension in non-drinkers: a possible role of fatty liver in the pathogenesis of obesity related hypertension. Obes Res. 1993; 1: 469–474.[Medline] [Order article via Infotrieve]
44. Robinson D, Whitehead TP. Effect of body mass and other factors on serum liver enzyme levels in men attending for well population screening. Ann Clin Biochem. 1989; 26 (Pt 5): 393–400.[Medline] [Order article via Infotrieve]
45. Stranges S, Trevisan M, Dorn JM, Dmochowski J, Donahue RP. Body fat distribution, liver enzymes, and risk of hypertension: evidence from the Western New York Study. Hypertension. 2005; 46: 1186–1193.Epub 2005 Oct 3.
46. Lee DH, Jacobs DR Jr, Gross M, Steffes M. Serum gamma-glutamyltransferase was differently associated with microalbuminuria by status of hypertension or diabetes: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Clin Chem. 2005; 51: 1185–1191.
47. Lee DH, Ha MH, Kim KY, Jin DG, Jacobs DR Jr. Gamma-glutamyltransferase: an effect modifier in the association between age and hypertension in a 4-year follow-up study. J Hum Hypertens. 2004; 18: 803–807.[CrossRef][Medline] [Order article via Infotrieve]
48. Lee DH, Jacobs DR Jr, Gross M, Kiefe CI, Roseman J, Lewis CE, Steffes M. Gamma-glutamyltransferase is a predictor of incident diabetes and hypertension: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Clin Chem. 2003; 49: 1358–1366.
49. Ikai E, Honda R, Yamada Y. Serum gamma-glutamyl transpeptidase level and blood pressure in nondrinkers: a possible pathogenetic role of fatty liver in obesity-related hypertension. J Hum Hypertens. 1994; 8: 95–100.[Medline] [Order article via Infotrieve]
50. Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC Jr, Spertus JA, Costa F; Am Heart Association; National Heart, Lung, and Blood Institute. Related Articles, Links Diagnosis and management of the metabolic syndrome: an Am Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005; 112: 2735–2752.
51. Tracy RP. Inflammation, the metabolic syndrome and cardiovascular risk. Int J Clin Pract Suppl. 2003; 134: 10–17.[Medline] [Order article via Infotrieve]
52. Palomo I, Alarcon M, Moore-Carrasco R, Argiles JM. Hemostasis alterations in metabolic syndrome (review). Int J Mol Med. 2006; 18: 969–974.[Medline] [Order article via Infotrieve]
53. Trayhurn P. Endocrine and signalling role of adipose tissue: new perspectives on fat. Acta Physiol Scand. 2005; 184: 285–293.[CrossRef][Medline] [Order article via Infotrieve]
54. Reaven GM. Insulin resistance, the insulin resistance syndrome, and cardiovascular disease. Panminerva Med. 2005; 47: 201–210.[Medline] [Order article via Infotrieve]
55. Heald AH, Kaushal K, Siddals KW, Rudenski AS, Anderson SG, Gibson JM. Insulin-like growth factor binding protein-2 (IGFBP-2) is a marker for the metabolic syndrome. Exp Clin Endocrinol Diabetes. 2006; 114: 371–376.[CrossRef][Medline] [Order article via Infotrieve]
56. Sesti G, Sciacqua A, Cardellini M, Marini MA, Maio R, Vatrano M, Succurro E, Lauro R, Federici M, Perticone F. Plasma concentration of IGF-I is independently associated with insulin sensitivity in subjects with different degrees of glucose tolerance. Diabetes Care. 2005; 28: 120–125.
57. Ridker PM, Wilson PW, Grundy SM. Related Articles, Links Should C-reactive protein be added to metabolic syndrome and to assessment of global cardiovascular risk? Circulation. 2004; 109: 2818–2825.
58. Browning LM, Jebb SA, Mishra GD, Cooke JH, O’Connell MA, Crook MA, Krebs JD. Elevated sialic acid, but not CRP, predicts features of the metabolic syndrome independently of BMI in women. Int J Obes Relat Metab Disord. 2004; 28: 1004–1010.[CrossRef][Medline] [Order article via Infotrieve]
59. Salonen JT. Uric acid level as a risk factor for cardiovascular and all-cause mortality in middle-aged men: a prospective cohort study. Arch Intern Med. 2004; 164: 1546–1551.
60. Gonzalez AS, Guerrero DB, Soto MB, Diaz SP, Martinez-Olmos M, Vidal O. Metabolic syndrome, insulin resistance and the inflammation markers C-reactive protein and ferritin. Eur J Clin Nutr. 2006; 60: 802–809.[CrossRef][Medline] [Order article via Infotrieve]
61. Jehn M, Clark JM, Guallar E. Serum ferritin and risk of the metabolic syndrome in U.S. adults. Diabetes Care. 2004; 27: 2422–2428.
62. Glintborg D, Andersen M, Hagen C, Frystyk J, Hulstrom V, Flyvbjerg A, Hermann AP. Evaluation of metabolic risk markers in polycystic ovary syndrome (PCOS). Adiponectin, ghrelin, leptin and body composition in hirsute PCOS patients and controls. Eur J Endocrinol. 2006; 155: 337–345.
63. Lewis JG, Shand BI, Elder PA, Scott RS. Plasma sex hormone-binding globulin rather than corticosteroid-binding globulin is a marker of insulin resistance in obese adult males. Diabetes Obes Metab. 2004; 6: 259–263.[CrossRef][Medline] [Order article via Infotrieve]
64. Olivieri O, Bassi A, Stranieri C, Trabetti E, Martinelli N, Pizzolo F, Girelli D, Friso S, Pignatti PF, Corrocher R. Apolipoprotein C-III, metabolic syndrome, and risk of coronary artery disease. J Lipid Res. 2003; 44: 2374–2378.
65. Handberg A, Levin K, Hojlund K, Beck-Nielsen H. Identification of the oxidized low-density lipoprotein scavenger receptor CD36 in plasma: a novel marker of insulin resistance. Circulation. 2006; 114: 1169–1176.
66. Gokulakrishnan K, Deepa R, Mohan V, Gross MD. Soluble P-selectin and CD40L levels in subjects with prediabetes, diabetes mellitus, and metabolic syndrome–the Chennai Urban Rural Epidemiology Study. Metabolism. 2006; 55: 237–242.[CrossRef][Medline] [Order article via Infotrieve]
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