Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass

Abstract The apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic β-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing...

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Autores principales:	Brenda Strutt, Sandra Szlapinski, Thineesha Gnaneswaran, Sarah Donegan, Jessica Hill, Jamie Bennett, David J. Hill
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/246c2beb3c1a49a7967a8f0091bbb0e0
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spelling	oai:doaj.org-article:246c2beb3c1a49a7967a8f0091bbb0e02021-12-02T16:31:52ZOntology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass10.1038/s41598-021-94725-02045-2322https://doaj.org/article/246c2beb3c1a49a7967a8f0091bbb0e02021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94725-0https://doaj.org/toc/2045-2322Abstract The apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic β-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing, glucose transporter 2-low (Ins+Glut2LO) progenitor cells. We examined changes in the apelinergic system during normal mouse pregnancy and in pregnancies complicated by glucose intolerance with reduced BCM. Expression of Aplnr, Apelin and Apela was quantified in Ins+Glut2LO cells isolated from mouse pancreata and found to be significantly higher than in mature β-cells by DNA microarray and qPCR. Apelin was localized to most β-cells by immunohistochemistry although Aplnr was predominantly associated with Ins+Glut2LO cells. Aplnr-staining cells increased three- to four-fold during pregnancy being maximal at gestational days (GD) 9–12 but were significantly reduced in glucose intolerant mice. Apelin-13 increased β-cell proliferation in isolated mouse islets and INS1E cells, but not glucose-stimulated insulin secretion. Glucose intolerant pregnant mice had significantly elevated serum Apelin levels at GD 9 associated with an increased presence of placental IL-6. Placental expression of the apelinergic axis remained unaltered, however. Results show that the apelinergic system is highly expressed in pancreatic β-cell progenitors and may contribute to β-cell proliferation in pregnancy.Brenda StruttSandra SzlapinskiThineesha GnaneswaranSarah DoneganJessica HillJamie BennettDavid J. HillNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Brenda Strutt Sandra Szlapinski Thineesha Gnaneswaran Sarah Donegan Jessica Hill Jamie Bennett David J. Hill Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
description	Abstract The apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic β-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing, glucose transporter 2-low (Ins+Glut2LO) progenitor cells. We examined changes in the apelinergic system during normal mouse pregnancy and in pregnancies complicated by glucose intolerance with reduced BCM. Expression of Aplnr, Apelin and Apela was quantified in Ins+Glut2LO cells isolated from mouse pancreata and found to be significantly higher than in mature β-cells by DNA microarray and qPCR. Apelin was localized to most β-cells by immunohistochemistry although Aplnr was predominantly associated with Ins+Glut2LO cells. Aplnr-staining cells increased three- to four-fold during pregnancy being maximal at gestational days (GD) 9–12 but were significantly reduced in glucose intolerant mice. Apelin-13 increased β-cell proliferation in isolated mouse islets and INS1E cells, but not glucose-stimulated insulin secretion. Glucose intolerant pregnant mice had significantly elevated serum Apelin levels at GD 9 associated with an increased presence of placental IL-6. Placental expression of the apelinergic axis remained unaltered, however. Results show that the apelinergic system is highly expressed in pancreatic β-cell progenitors and may contribute to β-cell proliferation in pregnancy.
format	article
author	Brenda Strutt Sandra Szlapinski Thineesha Gnaneswaran Sarah Donegan Jessica Hill Jamie Bennett David J. Hill
author_facet	Brenda Strutt Sandra Szlapinski Thineesha Gnaneswaran Sarah Donegan Jessica Hill Jamie Bennett David J. Hill
author_sort	Brenda Strutt
title	Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
title_short	Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
title_full	Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
title_fullStr	Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
title_full_unstemmed	Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
title_sort	ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/246c2beb3c1a49a7967a8f0091bbb0e0
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Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass

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