Non-alcoholic fatty liver disease and subclinical atherosclerosis: A comparison of metabolically-versus genetically-driven excess fat hepatic storage

Abstract Background and aims Non-alcoholic fatty liver disease (NAFLD) is frequently associated with atherosclerosis. However, it is unclear whether this association is related to excess fat liver storage per se or to metabolic abnormalities that typically accompany NAFLD. To investigate this, we co...

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Veröffentlicht in:Atherosclerosis 2017-02, Vol.257, p.232-239
Hauptverfasser: Di Costanzo, Alessia, D'Erasmo, Laura, Polimeni, Licia, Baratta, Francesco, Coletta, Paola, Di Martino, Michele, Loffredo, Lorenzo, Perri, Ludovica, Ceci, Fabrizio, Montali, Anna, Girelli, Gabriella, De Masi, Bruna, Angeloni, Antonio, Catalano, Carlo, Maranghi, Marianna, Del Ben, Maria, Angelico, Francesco, Arca, Marcello
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Sprache:eng
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Zusammenfassung:Abstract Background and aims Non-alcoholic fatty liver disease (NAFLD) is frequently associated with atherosclerosis. However, it is unclear whether this association is related to excess fat liver storage per se or to metabolic abnormalities that typically accompany NAFLD. To investigate this, we compared individuals with hepatic steatosis driven by metabolic disturbances to those with hepatic steatosis associated with the rs738409 GG genotype in the patatin-like phospholipase domain-containing 3 gene ( PNPLA3 ). Methods Carotid intima-media thickness (CIMT), as a surrogate marker of subclinical atherosclerosis, was measured in 83 blood donors with the mutant GG genotype (group G), 100 patients with features of metabolic syndrome (MetS) but the wildtype CC genotype (group M), and 74 blood donors with the wildtype CC genotype (controls). Fatty liver was evaluated by ultrasonography and hepatic fat fraction (HFF) was measured using magnetic resonance (MRS/MRI) in 157 subjects. Results Compared with group G and controls, group M subjects were older and had increased adiposity indices, dyslipidemia, insulin resistance and elevated transaminase levels (all p  
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2016.12.018