dc.contributor.author |
Bloomfield, Francis |
en |
dc.date.accessioned |
2020-01-12T20:53:22Z |
en |
dc.date.issued |
2018-09 |
en |
dc.identifier.issn |
0022-0795 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/49503 |
en |
dc.description.abstract |
As increasing numbers of babies born preterm survive into adulthood, it is becoming clear that, in addition to the well-described risks of neurodevelopmental sequelae, there also are increased risks for non-communicable diseases, including diabetes. Epidemiological studies indicate that risks are increased even for birth at late preterm and early term gestations and for both type 1 and type 2 diabetes. Thus, factors related to preterm birth likely affect development of the fetal and neonatal beta-cell in addition to effects on peripheral insulin sensitivity. These factors could operate prior to preterm birth and be related to the underlying cause of preterm birth, to the event of being born preterm itself, to the postnatal care of the preterm neonate or to a combination of these exposures. Experimental evidence indicates that factors may be operating during all these critical periods to contribute to altered development of beta-cell mass in those born preterm. Greater understanding of how these factors impact upon development of the pancreas may lead to interventions or management approaches that mitigate the increased risk of later diabetes. |
en |
dc.format.medium |
Print-Electronic |
en |
dc.language |
eng |
en |
dc.relation.ispartofseries |
The Journal of endocrinology |
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. |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.subject |
Islets of Langerhans |
en |
dc.subject |
Humans |
en |
dc.subject |
Premature Birth |
en |
dc.subject |
Infant, Premature, Diseases |
en |
dc.subject |
Diabetes Mellitus, Type 2 |
en |
dc.subject |
Risk Factors |
en |
dc.subject |
Pregnancy |
en |
dc.subject |
Infant, Newborn |
en |
dc.subject |
Infant, Premature |
en |
dc.subject |
Female |
en |
dc.subject |
Insulin-Secreting Cells |
en |
dc.title |
Impact of prematurity for pancreatic islet and beta-cell development. |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1530/joe-18-0021 |
en |
pubs.issue |
3 |
en |
pubs.begin-page |
R161 |
en |
pubs.volume |
238 |
en |
dc.rights.holder |
Copyright: The author |
en |
pubs.end-page |
R171 |
en |
pubs.publication-status |
Published |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.subtype |
Review |
en |
pubs.subtype |
Journal Article |
en |
pubs.elements-id |
752803 |
en |
pubs.org-id |
Liggins Institute |
en |
pubs.org-id |
LiFePATH |
en |
dc.identifier.eissn |
1479-6805 |
en |
pubs.record-created-at-source-date |
2018-06-14 |
en |
pubs.dimensions-id |
29895718 |
en |