Gestational Diabetes Adversely Affects Pancreatic Islet Architecture and Function in the Male Rat Offspring
Open accessAbstract
Fetal exposure to gestational diabetes mellitus (GDM) and poor postnatal diet are strong risk factors for type 2 diabetes development later in life, but the mechanisms connecting GDM exposure to offspring metabolic health remains unclear. In this study, we aimed to determine how GDM interacts with the postnatal diet to affect islet function in the offspring as well as characterize the gene expression changes in the islets. GDM was induced in female rats using a high-fat, high-sucrose (HFS) diet, and litters from lean or GDM dams were weaned onto a low-fat (LF) or HFS diet. Compared with the lean control offspring, GDM exposure reduced glucose-stimulated insulin secretion in islets isolated from 15-week-old offspring, which was additively worsened when GDM exposure was combined with postnatal HFS diet consumption. In the HFS diet–fed offspring of lean dams, islet size and number increased, an adaptation that was not observed in the HFS diet–fed offspring of GDM dams. Islet gene expression in the offspring of GDM dams was altered in such categories as inflammation (e.g., Il1b, Ccl2), mitochondrial function/oxidative stress resistance (e.g., Atp5f1, Sod2), and ribosomal proteins (e.g., Rps6, Rps14). These results demonstrate that GDM exposure induced marked changes in gene expression in the male young adult rat offspring that cumulatively interact to worsen islet function, whole-body glucose homeostasis, and adaptations to HFS diets.
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Gestational diabetes mellitus exposure conditioned 3-month-old offspring to the development of obesity, hepatic steatosis, glucose intolerance and pancreatic islet dysfunction.
“we demonstrated that GDM exposure conditioned 3-month-old offspring to the development of obesity, hepatic steatosis, glucose intolerance [102] and pancreatic islet dysfunction [103,104] (Figure 1).”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [103]
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Self-citation
- Authors
- Agarwal, P., Brar, N., Morriseau, T. S., Kereliuk, S. M., Fonseca, M. A., Cole, L. K., Jha, A., Xiang, B., Hunt, K. L., Seshadri, N., Hatch, G. M., Doucette, C. A., & Dolinsky, V. W.
- Affiliations
- Children's Hospital Research Institute of Manitoba (CA)
- University of Manitoba (CA)
- Corresponding author
- Doucette, Christine A
- Dolinsky, Vernon W
- ORCID
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2019-06-25
- Volume
- 160
- Issue
- 8
- Pages
- 1907-1925
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC6656426
- OpenAlex
- W2954143985
- Cited by
- 34
- References
- 35
- Citations by year
- 2026: 7 · 2025: 1 · 2024: 5 · 2023: 7 · 2022: 7 · 2021: 2 · 2020: 4 · 2019: 1
- FWCI
- 3.34
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (144626, 136885)
- Research Manitoba
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- gestational diabetes mellitus, pancreatic islets, islet architecture, glucose-stimulated insulin secretion, type 2 diabetes risk, islet gene expression, insulitis, oxidative stress, mitochondrial function, ribosomal proteins, glucose homeostasis, developmental programming, male offspring, rat model
- MeSH terms
- Animals, Body Weight, Female, Glucose, Islets of Langerhans, Male, Pregnancy, Sucrose, Gene Expression, Diabetes, Gestational, Rats, Sprague-Dawley, Rats, Diet, High-Fat
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