Genetic disruption of the Gipr in Apoe^-/- mice promotes atherosclerosis.

ABSTRACT:

Objective

The gut hormone glucose-dependent insulinotropic polypeptide (GIP) stimulates beta cell function and improves glycemia through its incretin actions. GIP also regulates endothelial function and suppresses adipose tissue inflammation through control of macrophage activity. Activation of the GIP receptor (GIPR) attenuates experimental atherosclerosis and inflammation in mice, however whether loss of GIPR signaling impacts the development of atherosclerosis is uncertain.

Methods

Atherosclerosis and related metabolic phenotypes were studied in Apoe^-/-:Gipr^-/- mice and in Gipr^+/+ and Gipr^-/- mice treated with an adeno-associated virus expressing PCSK9 (AAV-PCSK9). Bone marrow transplantation (BMT) studies were carried out using

SUBMITTER: Pujadas G 

PROVIDER: S-EPMC9478451 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature