On this background of evidence, the results of the study by Di Costanzo et al. [8] provide further support to the view that the aetiology of NAFLD is multifactorial and this disease may be caused by common genetic variants. One of these, the PNPLA-3 variant, is associated with higher liver fat content and increased risk of NASH, but is not systematically associated with insulin resistance and MetS traits [4,5]. This study adds a further critical piece of information by suggesting that the MetS-related NAFLD and the PNPLA3-related NAFLD may differentially affect the risk of subclinical atherosclerosis and perhaps of clinical CVD [8]. However, it does not detract from the notion that NAFLD, especially NASH with varying degrees of fibrosis, may directly contribute to the development and progression of CVD [2,3,9], because genetic NAFLD is a subtly different disease and less than 15% of European patients with NAFLD have the PNPLA3 GG genotype [4,5]. Furthermore, as previously mentioned, the few observational studies that have assessed the association between the PNPLA3 rs738409 gene polymorphism and risk of atherosclerosis have provided conflicting results (as summarized in Table 1)

"Not all forms of NAFLD were created equal". Do metabolic syndrome-related NAFLD and PNPLA3-related NAFLD exert a variable impact on the risk of early carotid atherosclerosis?

TARGHER, Giovanni
2017-01-01

Abstract

On this background of evidence, the results of the study by Di Costanzo et al. [8] provide further support to the view that the aetiology of NAFLD is multifactorial and this disease may be caused by common genetic variants. One of these, the PNPLA-3 variant, is associated with higher liver fat content and increased risk of NASH, but is not systematically associated with insulin resistance and MetS traits [4,5]. This study adds a further critical piece of information by suggesting that the MetS-related NAFLD and the PNPLA3-related NAFLD may differentially affect the risk of subclinical atherosclerosis and perhaps of clinical CVD [8]. However, it does not detract from the notion that NAFLD, especially NASH with varying degrees of fibrosis, may directly contribute to the development and progression of CVD [2,3,9], because genetic NAFLD is a subtly different disease and less than 15% of European patients with NAFLD have the PNPLA3 GG genotype [4,5]. Furthermore, as previously mentioned, the few observational studies that have assessed the association between the PNPLA3 rs738409 gene polymorphism and risk of atherosclerosis have provided conflicting results (as summarized in Table 1)
Atherosclerosis; Carotid; Genetic polymorphisms; Insulin resistance; Metabolic syndrome; NAFLD
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/958573
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