The cardiac hormones atrial (ANP) and B-type natriuretic peptides (BNP) moderate arterial blood pressure and improve energy metabolism as well as insulin sensitivity via their shared cGMP-producing guanylyl cyclase-A (GC-A) receptor. Obesity is associated with impaired NP/GC-A/cGMP signaling, which possibly contributes to the development of type 2 diabetes and its cardiometabolic complications. In vitro, synthetic ANP, via GC-A, stimulates glucose-dependent insulin release from cultured pancreatic islets and β-cell proliferation. However, the relevance for systemic glucose homeostasis in vivo is not known. To dissect whether the endogenous cardiac hormones modulate the secretory function and/or proliferation of β-cells under (patho)physiological conditions in vivo, here we generated a novel genetic mouse model with selective disruption of the GC-A receptor in β-cells.
%0 Journal Article
%1 tauscher2018cellspecific
%A Tauscher, Sabine
%A Nakagawa, Hitoshi
%A Völker, Katharina
%A Werner, Franziska
%A Krebes, Lisa
%A Potapenko, Tamara
%A Doose, Sören
%A Birkenfeld, Andreas L.
%A Baba, Hideo A.
%A Kuhn, Michaela
%B 1
%D 2018
%J Cardiovascular Diabetology
%K doose
%P 103
%T β Cell-specific deletion of guanylyl cyclase A, the receptor for atrial natriuretic peptide, accelerates obesity-induced glucose intolerance in mice
%U https://doi.org/10.1186/s12933-018-0747-3
%V 17
%X The cardiac hormones atrial (ANP) and B-type natriuretic peptides (BNP) moderate arterial blood pressure and improve energy metabolism as well as insulin sensitivity via their shared cGMP-producing guanylyl cyclase-A (GC-A) receptor. Obesity is associated with impaired NP/GC-A/cGMP signaling, which possibly contributes to the development of type 2 diabetes and its cardiometabolic complications. In vitro, synthetic ANP, via GC-A, stimulates glucose-dependent insulin release from cultured pancreatic islets and β-cell proliferation. However, the relevance for systemic glucose homeostasis in vivo is not known. To dissect whether the endogenous cardiac hormones modulate the secretory function and/or proliferation of β-cells under (patho)physiological conditions in vivo, here we generated a novel genetic mouse model with selective disruption of the GC-A receptor in β-cells.
@article{tauscher2018cellspecific,
abstract = {The cardiac hormones atrial (ANP) and B-type natriuretic peptides (BNP) moderate arterial blood pressure and improve energy metabolism as well as insulin sensitivity via their shared cGMP-producing guanylyl cyclase-A (GC-A) receptor. Obesity is associated with impaired NP/GC-A/cGMP signaling, which possibly contributes to the development of type 2 diabetes and its cardiometabolic complications. In vitro, synthetic ANP, via GC-A, stimulates glucose-dependent insulin release from cultured pancreatic islets and β-cell proliferation. However, the relevance for systemic glucose homeostasis in vivo is not known. To dissect whether the endogenous cardiac hormones modulate the secretory function and/or proliferation of β-cells under (patho)physiological conditions in vivo, here we generated a novel genetic mouse model with selective disruption of the GC-A receptor in β-cells.
},
added-at = {2018-12-18T14:13:02.000+0100},
author = {Tauscher, Sabine and Nakagawa, Hitoshi and Völker, Katharina and Werner, Franziska and Krebes, Lisa and Potapenko, Tamara and Doose, Sören and Birkenfeld, Andreas L. and Baba, Hideo A. and Kuhn, Michaela},
biburl = {https://www.bibsonomy.org/bibtex/23bc7a0c0c71b4165fd7c5fce5f129115/reichert},
interhash = {04977917d1d9482b70a5f5c4ee9eeb1c},
intrahash = {3bc7a0c0c71b4165fd7c5fce5f129115},
issn = {1475-2840},
journal = {Cardiovascular Diabetology},
keywords = {doose},
pages = 103,
series = 1,
timestamp = {2018-12-18T14:13:02.000+0100},
title = {β Cell-specific deletion of guanylyl cyclase A, the receptor for atrial natriuretic peptide, accelerates obesity-induced glucose intolerance in mice},
url = {https://doi.org/10.1186/s12933-018-0747-3},
volume = 17,
year = 2018
}