December 2020

Volume 61Issue 12p1537-1790
Open Access
COVER: Oxysterol accumulation drives NAFL to NASH. In early fatty liver, lowered hepatocellular insulin levels (i.e., insulin resistance) suppress CYP7B1 expression and promote oxysterol accumulation. Chronic persistent increase in (25R)-26-hydroxycholesterol (26-HC) with Western-diet feeding promotes further accumulation of 26-HC and its lipotoxic metabolites (i.e., 3β-hydroxy-5-cholestenoic acid, 3βHCA) as occurs in humans in the absence of CYP7B1. (See Kakiyama et al., p. 1629.)...
COVER: Oxysterol accumulation drives NAFL to NASH. In early fatty liver, lowered hepatocellular insulin levels (i.e., insulin resistance) suppress CYP7B1 expression and promote oxysterol accumulation. Chronic persistent increase in (25R)-26-hydroxycholesterol (26-HC) with Western-diet feeding promotes further accumulation of 26-HC and its lipotoxic metabolites (i.e., 3β-hydroxy-5-cholestenoic acid, 3βHCA) as occurs in humans in the absence of CYP7B1. (See Kakiyama et al., p. 1629.)

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