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Research Article

Association of liver enzymes with metabolic syndrome and carotid atherosclerosis in young adults. The Cardiovascular Risk in Young Finns Study

, , , , , , , , , & show all
Pages 187-195 | Received 03 Jul 2010, Accepted 12 Oct 2010, Published online: 24 Jan 2011
 

Abstract

Objective. We examined whether metabolic syndrome (MetS) predicts increased alanine aminotransferase (ALT) and gamma-glutamyltransferase (GGT) levels in young adults, whether spontaneous recovery from MetS has a favorable effect on liver enzyme activities, and whether these enzymes contribute to the atherogenicity of MetS (assessed by carotid intima-media thickness (IMT)).

Methods. The study included 1,553 subjects (base-line age 31.5 ± 5.0 years). ALT and GGT were measured in 2007. MetS was diagnosed by the new Joint Interim Societies definition.

Results. ALT and GGT levels were higher in subjects with MetS compared to those without in 2007. The association was independent of alcohol intake and BMI. In multivariable models adjusted for base-line age, LDL cholesterol, CRP, alcohol intake, and adiponectin, MetS in 2001 predicted increased ALT (β ± SEM = 0.320 ± 0.062, P < 0.0001 in men; 0.134 ± 0.059, P = 0.02 in women) and GGT (β ± SEM = 0.222 ± 0.067, P < 0.0001 in men; 0.236 ± 0.060, P < 0.0001 in women) levels after 6 years. Subjects with MetS only at base-line (2001) had lower ALT levels after 6 years compared to subjects with persistent and incident MetS. No statistically significant interaction for MetS*ALT (P = 0.81) or MetS*GGT (P = 0.92) on IMT was observed.

Conclusion. In young adults MetS may induce liver enzyme changes that indicate increased risk of non-alcoholic fatty liver disease, but we found no evidence that increased enzyme levels would amplify the atherogenicity of MetS.

Declaration of interest: This study was financially supported by the Academy of Finland (grant no. 117797, 121584, 126925), Turku University, the Turku University Foundation, the Tampere University Hospital Medical Fund, the Finnish Foundation of Cardiovascular Research, the Lydia Maria Julin Foundation, Juho Vainio Foundation, Finnish Cultural Foundation, Finnish Medical Foundation, and Research Foundation of Orion Corporation. The authors declare no conflicts of interest.

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