Commentary
Longitudinal observations were performed by C. Chen et al. in a cohort of 2,811 participants with no liver disease at inception. The rate of the conversion to NAFLD was 15.7%, with a steady increase in prevalence observed in sub-cohorts with increasing HbA1c levels.
The results suggest that increased levels of HbA1c may contribute to the progression of NAFLD either directly, by stimulating receptor for advanced glycation end products (RAGE), or indirectly, through the promotion of hypoxia and suppression of the release of NO.
