Consequence of PCSK9 deficiency in obese mice after a Roux en Y gastric by-pass

Background and Aims: The Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a master regulator of Low Density Lipoprotein Cholesterol (LDL-C) metabolism, acting as an endogenous inhibitor of the LDL receptor. In 2018, we observed that Roux en Y Gastric Bypass (RYGB) in mice induces an intestinal mucosa hypertrophy and is associated with a strong increase of intestinal PCSK9 mRNA levels. By analogy with its critical role in liver regeneration after hepatectomy, we emphasized that PCSK9 expression up-regulation is physiologically important after RYGB to promote the intestinal wall thickening for improving nutrients absorption. Here, we investigated the consequences of PCSK9 deficiency in DIO mice after a sham or RYGB surgery.