A study found that the TG and CHOL of the Gilbert syndrome population were significantly lower than those of the normal population68, and it was found that the homozygous recessive Gunn rats (UGT1A1 deficiency resulted in higher bilirubin levels in the body, and the homozygous recessive rats had the highest bilirubin levels), and the body weight is also lighter than that of the littermates69, which indicates that the elevated bilirubin level caused by the mutation of the bilirubin metabolism-related gene can prevent the lipid metabolism disorder to a certain extent. Here, UGT1A1 is linked to Disorder of lipid metabolism.