Absence of a gestational diabetes phenotype in the LepRdb/+ mouse is independent of control strain, diet, misty allele, or parity

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dc.contributor.author Plows, Jasmine en
dc.contributor.author Yu, X en
dc.contributor.author Broadhurst, R en
dc.contributor.author Vickers, Mark en
dc.contributor.author Tong, C en
dc.contributor.author Zhang, H en
dc.contributor.author Qi, H en
dc.contributor.author Stanley, JL en
dc.contributor.author Baker, Philip en
dc.date.accessioned 2017-08-30T00:53:39Z en
dc.date.issued 2017-03-24 en
dc.identifier.citation Scientific Reports 7:45130 24 Mar 2017 en
dc.identifier.issn 2045-2322 en
dc.identifier.uri http://hdl.handle.net/2292/35404 en
dc.description.abstract Treatment options for gestational diabetes (GDM) are limited. In order to better understand mechanisms and improve treatments, appropriate animal models of GDM are crucial. Heterozygous db mice (db/+) present with glucose intolerance, insulin resistance, and increased weight gain during, but not prior to, pregnancy. This makes them an ideal model for GDM. However, several recent studies have reported an absence of GDM phenotype in their colony. We investigated several hypotheses for why the phenotype may be absent, with the aim of re-establishing it and preventing further resources being wasted on an ineffective model. Experiments were carried out across two laboratories in two countries (New Zealand and China), and were designed to assess type of control strain, diet, presence of the misty allele, and parity as potential contributors to the lost phenotype. While hyperleptinemia and pre-pregnancy weight gain were present in all db/+mice across the four studies, we found no consistent evidence of glucose intolerance or insulin resistance during pregnancy. In conclusion, we were unable to acquire the GDM phenotype in any of our experiments, and we recommend researchers do not use the db/+ mouse as a model of GDM unless they are certain the phenotype remains in their colony. en
dc.format.medium Electronic en
dc.language eng en
dc.publisher Nature Publishing Group en
dc.relation.ispartofseries Scientific Reports en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://www.sherpa.ac.uk/romeo/issn/2045-2322/ en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.rights.uri https://creativecommons.org/licenses/by/4.0/ en
dc.title Absence of a gestational diabetes phenotype in the LepRdb/+ mouse is independent of control strain, diet, misty allele, or parity en
dc.type Journal Article en
dc.identifier.doi 10.1038/srep45130 en
pubs.volume 7 en
dc.description.version VoR - Version of Record en
dc.rights.holder Copyright: The authors en
dc.identifier.pmid 28338021 en
dc.rights.accessrights http://purl.org/eprint/accessRights/OpenAccess en
pubs.subtype Article en
pubs.elements-id 619044 en
pubs.org-id Liggins Institute en
dc.identifier.eissn 2045-2322 en
pubs.number 45130 en
pubs.record-created-at-source-date 2017-08-30 en
pubs.dimensions-id 28338021 en

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