Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome.

ABSTRACT:

Objective

Endothelin receptor B (ETB) together with ETA mediates cellular effects of endothelin 1 (ET-1), an autocrine and endocrine peptide produced by the endothelium and other cells. It regulates vascular tone and controls kidney function. Metabolic syndrome is due to high caloric intake and is characterized by insulin resistance, dyslipidemia, and white adipose tissue (WAT) accumulation. ETA/ETB antagonism has been demonstrated to favorably influence insulin resistance. Our study explored the role of ETB in metabolic syndrome.

Methods

Wild type (etb^+/+) and rescued ETB-deficient (etb^-/-) mice were fed a high-fat diet, and energy, glucose, and insulin metabolism were analyzed, and hormones and lipids measured in serum and tissues. Cell culture experi

SUBMITTER: Feger M 

PROVIDER: S-EPMC10825011 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature