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Inactivation of the Glucose-Dependent Insulinotropic Polypeptide Receptor Improves Outcomes following Experimental Myocardial Infarction.

Abstract：

:Incretin hormones exert pleiotropic metabolic actions beyond the pancreas. Although the heart expresses both incretin receptors, the cardiac biology of GIP receptor (GIPR) action remains incompletely understood. Here we show that GIPR agonism did not impair the response to cardiac ischemia. In contrast, genetic elimination of the Gipr reduced myocardial infarction (MI)-induced ventricular injury and enhanced survival associated with reduced hormone sensitive lipase (HSL) phosphorylation; it also increased myocardial triacylglycerol (TAG) stores. Conversely, direct GIPR agonism in the isolated heart reduced myocardial TAG stores and increased fatty acid oxidation. The cardioprotective phenotype in Gipr-/- mice was partially reversed by pharmacological activation or genetic overexpression of HSL. Selective Gipr inactivation in cardiomyocytes phenocopied Gipr-/- mice, resulting in improved survival and reduced adverse remodeling following experimental MI. Hence, the cardiomyocyte GIPR regulates fatty acid metabolism and the adaptive response to ischemic cardiac injury. These findings have translational relevance for developing GIPR-based therapeutics.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

Ussher JR,Campbell JE,Mulvihill EE,Baggio LL,Bates HE,McLean BA,Gopal K,Capozzi M,Yusta B,Cao X,Ali S,Kim M,Kabir MG,Seino Y,Suzuki J,Drucker DJ

doi

10.1016/j.cmet.2017.11.003

subject

Has Abstract

pub_date

2018-02-06 00:00:00

pages

450-460.e6

issue

2

eissn

1550-4131

issn

1932-7420

pii

S1550-4131(17)30671-X

journal_volume

27

pub_type

杂志文章

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