We read with great interest the article by Nelson et al. The authors elegantly described the association between patterns of in-trahepatic iron deposition (within the hepatocytes [HC]; in the reticular endothelial cells [RES]; or both, HC/RES), liver histology, and metabolic abnormalities, including dyslipidemia and insulin resistance in the large cohort of adult patients from the Non-Alcoholic Steatohepatitis Clinical Research Network (NASH-CNR). Intrahepatic iron deposition was found in 34.5% of patients. Most of them (44.7%) showed a mixed pattern, while the RES pattern was significantly associated with more severe histologi-cal damage and, particularly, with fibrosis. These findings seem to support the concept that differences may exist in patients with fatty liver based on different genetic background, inclination to inflammation, and co-occurrence of metabolic abnormalities such as diabetes. In this context, hepatic iron overload would represent a complex phenotype resulting from the maladaptation to environmental cues, mainly nutrients, and nurtured by metabolic abnormalities such as altered glucose metabolism (Fig. I).
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