A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics

Abstract Physiological changes during pregnancy support foetal growth, including adaptations in pancreatic islets to maintain glucose homeostasis. We investigate these adaptations using rare, high-quality pancreatic tissue from pregnant human donors and matched controls. We profile islets from pregn...

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Main Authors: Faheem Seedat, Katie Holden, Simon Davis, Roman Fischer, James Bancroft, Edward Drydale, Neva Kandzija, John A. Todd, Manu Vatish, M. Irina Stefana
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-61852-5
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author Faheem Seedat
Katie Holden
Simon Davis
Roman Fischer
James Bancroft
Edward Drydale
Neva Kandzija
John A. Todd
Manu Vatish
M. Irina Stefana
author_facet Faheem Seedat
Katie Holden
Simon Davis
Roman Fischer
James Bancroft
Edward Drydale
Neva Kandzija
John A. Todd
Manu Vatish
M. Irina Stefana
author_sort Faheem Seedat
collection DOAJ
description Abstract Physiological changes during pregnancy support foetal growth, including adaptations in pancreatic islets to maintain glucose homeostasis. We investigate these adaptations using rare, high-quality pancreatic tissue from pregnant human donors and matched controls. We profile islets from pregnant donors using proteomics and assess α- and β-cell characteristics, as well as prolactin receptor and serotonin 2B receptor expression. Proteomic profiling of microdissected human islets identifies 7546 proteins but shows minimal differences in protein expression. In pregnancy, we show that islet area increases 1.9-fold, α- and β-cell areas increase 4.3- and 1.9-fold, driven by an increase in cell number rather than hypertrophy. Prolactin receptor expression is higher in α but not β cells, and serotonin 2B receptor is undetectable in β cells. Glucagon-like peptide-1 abundance increases 2.9-fold in α cells. These findings indicate that the molecular mechanisms driving pregnancy-induced islet adaptations in humans differ from those in mice, highlighting the need for human-based studies.
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series Nature Communications
spelling doaj-art-d819dd250cd44351a5fe87192ae2c67c2025-08-20T03:46:12ZengNature PortfolioNature Communications2041-17232025-07-0116112310.1038/s41467-025-61852-5A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomicsFaheem Seedat0Katie Holden1Simon Davis2Roman Fischer3James Bancroft4Edward Drydale5Neva Kandzija6John A. Todd7Manu Vatish8M. Irina Stefana9Centre for Human Genetics, Nuffield Department of Medicine, University of OxfordCentre for Human Genetics, Nuffield Department of Medicine, University of OxfordTarget Discovery Institute, Centre for Medicines Discovery, Nuffield Department of Medicine, University of OxfordTarget Discovery Institute, Centre for Medicines Discovery, Nuffield Department of Medicine, University of OxfordCentre for Human Genetics, Nuffield Department of Medicine, University of OxfordCentre for Human Genetics, Nuffield Department of Medicine, University of OxfordNuffield Department of Women’s and Reproductive Health, University of OxfordCentre for Human Genetics, Nuffield Department of Medicine, University of OxfordCentre for Human Genetics, Nuffield Department of Medicine, University of OxfordCentre for Human Genetics, Nuffield Department of Medicine, University of OxfordAbstract Physiological changes during pregnancy support foetal growth, including adaptations in pancreatic islets to maintain glucose homeostasis. We investigate these adaptations using rare, high-quality pancreatic tissue from pregnant human donors and matched controls. We profile islets from pregnant donors using proteomics and assess α- and β-cell characteristics, as well as prolactin receptor and serotonin 2B receptor expression. Proteomic profiling of microdissected human islets identifies 7546 proteins but shows minimal differences in protein expression. In pregnancy, we show that islet area increases 1.9-fold, α- and β-cell areas increase 4.3- and 1.9-fold, driven by an increase in cell number rather than hypertrophy. Prolactin receptor expression is higher in α but not β cells, and serotonin 2B receptor is undetectable in β cells. Glucagon-like peptide-1 abundance increases 2.9-fold in α cells. These findings indicate that the molecular mechanisms driving pregnancy-induced islet adaptations in humans differ from those in mice, highlighting the need for human-based studies.https://doi.org/10.1038/s41467-025-61852-5
spellingShingle Faheem Seedat
Katie Holden
Simon Davis
Roman Fischer
James Bancroft
Edward Drydale
Neva Kandzija
John A. Todd
Manu Vatish
M. Irina Stefana
A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics
Nature Communications
title A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics
title_full A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics
title_fullStr A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics
title_full_unstemmed A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics
title_short A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics
title_sort new paradigm of islet adaptations in human pregnancy insights from immunohistochemistry and proteomics
url https://doi.org/10.1038/s41467-025-61852-5
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