Metabolic adaptations to pregnancy in healthy and gestational diabetic pregnancies: the pancreas - placenta Axis
Abstract
Normal pregnancy is associated with increased insulin resistance as a metabolic adaptation to the nutritional demands of the placenta and fetus, and this is amplified in obese mothers. Insulin resistance is normally compensated for by an adaptive increase in pancreatic β-cell mass together with enhanced glucose-stimulated insulin release. Placentally-derived hormones and growth factors are central to the altered pancreatic morphology and function. A failure of β-cells to undergo adaptive change after the first trimester has been linked with gestational diabetes. In the pregnant mouse, an increase in β-cell replication contributes to a 2-3-fold increase in mass peaking in late gestation, depending on the proliferation of existing β-cells, the differentiation of resident progenitor β-cells, or islet cell transdifferentiation. Using mouse models and human studies placenta- and islet of Langerhans-derived molecules have been identified that are likely to contribute to the metabolic adaptations to pregnancy and whose physiology is altered in the obese, glucose-intolerant mother. Maternal obesity during pregnancy can create a pro-inflammatory environment that can disrupt the response of the β-cells to the endocrine signals of pregnancy and limit the adaptive changes in β-cell mass and function, resulting in an increased risk of gestational diabetes.
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Gestational diabetes is characterized by increased insulin resistance and insufficient beta-cell insulin production.
“Another common pregnancy complication is gestational diabetes, characterized by increased insulin resistance and insufficient beta-cell insulin production (Szlapinski et al., 2021).”
From Pregnancy-related maternal physiological adaptations and fetal chemical exposure (2023) · cites this paper as Szlapinski et al., 2021
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Pregnancy-related maternal physiological adaptations and fetal chemical exposure
Vinnars, M.-T., Bixo, M., & Damdimopoulou, P. (2023) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2023.112064 · Cited by 32 · see citing works
- Authors
- Szlapinski, S. K., & Hill, D. J.
- Affiliations
- Lawson Health Research Institute (CA)
- Corresponding author
- Hill, David J.
- Venue
- Current Vascular Pharmacology
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2020-12-30
- Volume
- 19
- Issue
- 2
- Pages
- 141-153
- ISSN
- 1570-1611 (ISSN-L)
- OpenAlex
- W3012350505
- Cited by
- 56
- References
- 12
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 28 · 2023: 3 · 2022: 7 · 2021: 2 · 2020: 1
- FWCI
- 0.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Vascular Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (MOP-15263)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- pregnancy, gestational diabetes mellitus, insulin resistance, beta-cell mass, beta-cell proliferation, beta-cell transdifferentiation, placenta, placental hormones, pancreatic islets, maternal obesity, inflammation, glucose-stimulated insulin secretion, beta-cell function
- MeSH terms
- Pregnancy in Obesity, Adaptation, Physiological, Animals, Blood Glucose, Energy Metabolism, Female, Humans, Pancreas, Placenta, Pregnancy, Pregnancy Outcome, Risk Factors, Diabetes, Gestational, Oxidative Stress, Risk Assessment, Inflammation Mediators, Cell Proliferation, Insulin-Secreting Cells, Cell Transdifferentiation
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