Nonalcoholic fatty liver disease and metabolicsyndrome: Shared genetic basis of pathogenesis

CARLOS JOSE PIROLA; SILVIA SOOKOIAN

HEPATOLOGY (BALTIMORE, MD.)

JOHN WILEY & SONS INC

Lugar: New York; Año: 2016 vol. 64 p. 1417 - 1420

0270-9139

"Nature shows us only the tail of the lion. But I do not doubt that the lion belongs to it even though he cannot at once reveal himself because of his enormous size".-Albert Einstein. Growing body of evidence indicates that nonalcoholic fatty liver disease (NAFLD) develops from a complex process that includes genetic susceptibility and environmental exposure. Regardless of whether it is the cause or the consequence of the Metabolic Syndrome (MetS), NAFLD often co-occurs with one or more MetS-associated phenotypes. The robustness of the association is sufficient for making clinical decisions, such as assessment of concomitant cardiovascular disease (CVD), and implementation of lifestyle, or pharmacologic intervention to alleviate both NAFLD and the systemic metabolic picture (1). There is also robust evidence in support of NAFLD and MetS sharing common pathogenic mechanisms (1). Nevertheless, with the exception of TM6SF2 (2)?that illustrates an unexpected opposite association between NAFLD and CVD, although it can be suspected?no compelling report demonstrating that NAFLD and MetS share a common genetic background presently exists.