# NIH grant: Islet Function in Gestational Diabetes (1R01DK148528-01) — retained record

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source: [us-gov-api](https://highsignal.app/data/us-gov-api) (us-gov-api:nih-reporter)  published 2026-08-21 00:00 ingested 2026-08-24 06:48

[original source ↗](https://reporter.nih.gov/project-details/1R01DK148528-01)

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NIH grant 1R01DK148528-01: Islet Function in Gestational Diabetes
Institute: {'code': 'DK', 'abbreviation': 'NIDDK', 'name': 'National Institute of Diabetes and Digestive and Kidney Diseases', 'admin_org_id': '12500020', 'admin_funding_url': ''}. PI: Aoife Maria Egan. Award: $569882.
Start: 2026-08-21T00:00:00.
PROJECT SUMMARY/ABSTRACT
The overall aim of this application is to enhance our understanding of the pathophysiology of gestational
diabetes mellitus (GDM). GDM affects 8% pregnancies in the United States annually and increases the risk of
multiple adverse pregnancy outcomes including cesaresan delivery, large for gestational age infants, and
neonatal hypoglycemia. While the hyperglycemia associated with GDM resolves following delivery, >60% of
affected women develop type 2 diabetes (T2DM) or prediabetes by 10 years postpartum. These poor clinical
outcomes are underpinned by our incomplete understanding of the pathophysiology of GDM and postpartum
T2DM; conditions which are characterized by failure of the pancreatic islet cells to maintain normal glucose
concentrations. Prior studies examining pancreatic islet cell function in this population are limited and
predominantly focus on the β-cell, typically using surrogate markers. Our preliminary data identify the presence
of α-cell dysfunction in women with GDM both during pregnancy and postpartum. Furthermore, we provide
evidence of a role for intra-islet glucagon-like peptide-1 (GLP-1) in human pregnancy, a mechanism which may
be upregulated in the context of GDM-related islet stress (a phenomenon which is observed in T2DM). In the
proposed studies, we will assess α-cell (Aim 1) and β-cell (Aim 2) responses to varying degrees of
hyperglycemia in women with and without GDM and determine the relative contributions of α-cell and β-cell
dysfunction to the hyperglycemia observed in GDM. We will also examine the islet cell recovery (or lack
thereof) that occurs postpartum and determine the impact of lactation on this recovery. We will determine if
intra-islet GLP-1 contributes to glucose tolerance postpartum, and if this differs according to GDM or lactation
status (Aim 3). The experiments we propose will provide novel information about islet cell function during and
after pregnancy. In keeping with the NIDDK mission, the proposed work aims to unravel the complex
pathophysiology of GDM and postpartum T2DM, filling critical gaps in our knowledge and paving the way for
transformative advances in prevention and treatment.
```



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