Bilirubin deficiency renders mice susceptible to hepatic steatosis in the absence of insulin resistance.

ABSTRACT:

Background & aims

Plasma concentrations of bilirubin, a product of heme catabolism formed by biliverdin reductase A (BVRA), inversely associate with the risk of metabolic diseases including hepatic steatosis and diabetes mellitus in humans. Bilirubin has antioxidant and anti-inflammatory activities and may also regulate insulin signaling and peroxisome proliferator-activated receptor alpha (PPARα) activity. However, a causal link between bilirubin and metabolic diseases remains to be established. Here, we used the global Bvra gene knockout (Bvra^-/-) mouse as a model of deficiency in bilirubin to assess its role in metabolic diseases.

Approach & results

We fed mice fat-rich diets to induce hepatic steatosis and insulin resistance. Bile pigments were measured by LC-

SUBMITTER: Chen W 

PROVIDER: S-EPMC8498001 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature