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The primary driver of visceral obesity is an imbalance between intake and utilization of energy-dense metabolites (lipids and carbohydrates), the excess of which is converted to triacylglycerol (TAG) in the liver and in adipocytes [20,21]

The metabolomics data have been deposited to the EMBL-EBI MetaboLights database with the identifier MTBLS14139

Interestingly, in South America (Argentina and Venezuela), possession of the HLA DRB1*1301 allele, which does not conform to the shared motif model mentioned above, harbouring the sequence LIEDER at positions 6772 [44, 45, 57], not only does predispose to pediatric AIH-1 but is also associated with persistent infection with the endemic hepatitis A virus [43, 58]

The BPRF represents a conservative interpretation of the evidence, providing the smallest excess or reduced risk associated with alcohol consumption consistent with the data

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