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Cited by 128Pancreatic function and diabetesGestational Diabetes Research and ManagementBirth, Development, and Health

The DOI matches its Crossref record; 92 of the 93 references it cites were found in a registry or an index.

Maternal β-Cell Adaptations in Pregnancy and Placental Signalling: Implications for Gestational Diabetes

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Moyce, Brittany L., Dolinsky, Vernon W.·2018·International Journal of Molecular Sciences
DOI 10.3390/ijms19113467PMC PMC6274918
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Abstract

Rates of gestational diabetes mellitus (GDM) are on the rise worldwide, and the number of pregnancies impacted by GDM and resulting complications are also increasing. Pregnancy is a period of unique metabolic plasticity, during which mild insulin resistance is a physiological adaptation to prioritize fetal growth. To compensate for this, the pancreatic β-cell utilizes a variety of adaptive mechanisms, including increasing mass, number and insulin-secretory capacity to maintain glucose homeostasis. When insufficient insulin production does not overcome insulin resistance, hyperglycemia can occur. Changes in the maternal system that occur in GDM such as lipotoxicity, inflammation and oxidative stress, as well as impairments in adipokine and placental signalling, are associated with impaired β-cell adaptation. Understanding these pathways, as well as mechanisms of β-cell dysfunction in pregnancy, can identify novel therapeutic targets beyond diet and lifestyle interventions, insulin and antihyperglycemic agents currently used for treating GDM.

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Figure 1 Adaptations in peripheral tissue in late gestation occur to spare glucose for fetal growth; if insulin resistance is too severe (such as in pregnancies complicated by pre-existing obesity), gestational diabetes can occur.
Figure 1 Adaptations in peripheral tissue in late gestation occur to spare glucose for fetal growth; if insulin resistance is too severe (such as in pregnancies complicated by pre-existing obesity), gestational diabetes can occur.CC BY · PubMed Central
Figure 2 Signalling by pregnancy hormones prolactin (PrL) and placental lactogen (PL) through the prolactin receptor (PrlR) through the Jak/Stat pathway improves glucose stimulated insulin secretion (GSIS), prevents apoptosis and promotes proliferation and expansion. Hepatocyte growth factor (HGF) signals through AKT and mTOR via cMet to improve β-cell adaptations. Epidermal growth factor (EGF) through epidermal growth factor receptor (EGF-R) and ras/extracellular signal-related kinases (ERK) signalling can mediate proliferation and expansion; the ras/ERK pathway can also be mediated lactogens. Transcription factors (such as Hnf4a, FoxD3, FoxM1) can modulate expression of genes that mediate these adaptations.
Figure 2 Signalling by pregnancy hormones prolactin (PrL) and placental lactogen (PL) through the prolactin receptor (PrlR) through the Jak/Stat pathway improves glucose stimulated insulin secretion (GSIS), prevents apoptosis and promotes proliferation and expansion. Hepatocyte growth factor (HGF) signals through AKT and mTOR via cMet to improve β-cell adaptations. Epidermal growth factor (EGF) through epidermal growth factor receptor (EGF-R) and ras/extracellular signal-related kinases (ERK) signalling can mediate proliferation and expansion; the ras/ERK pathway can also be mediated lactogens. Transcription factors (such as Hnf4a, FoxD3, FoxM1) can modulate expression of genes that mediate these adaptations.CC BY · PubMed Central
Figure 3 Peripheral insulin resistance and resulting hyperlipidemia and hyperglycemia can overwhelm the capacity of the β-cell, leading to lipotoxicity and glucotoxicity. Lipotoxicity and glucotoxicity can trigger oxidative stress, generation of reactive oxygen species (ROS) and lead to endoplasmic reticulum (ER) stress and apoptosis; these detrimental pathways impair β-cell adaptation in pregnancy and can lead to gestational diabetes mellitus (GDM).
Figure 3 Peripheral insulin resistance and resulting hyperlipidemia and hyperglycemia can overwhelm the capacity of the β-cell, leading to lipotoxicity and glucotoxicity. Lipotoxicity and glucotoxicity can trigger oxidative stress, generation of reactive oxygen species (ROS) and lead to endoplasmic reticulum (ER) stress and apoptosis; these detrimental pathways impair β-cell adaptation in pregnancy and can lead to gestational diabetes mellitus (GDM).CC BY · PubMed Central

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Authors
Moyce, B. L., & Dolinsky, V. W.
Affiliations
  • Department of Pharmacology & Therapeutics and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Research Theme of the Children’s Hospital Research Institute of Manitoba and the Manitoba Developmental Origins of Chronic Diseases in Children Network (DEVOTION), University of Manitoba, Winnipeg, MB R3E 3P4, Canada
  • Children's Hospital Research Institute of Manitoba (CA)
Corresponding author
Dolinsky, Vernon W.
ORCID
Dolinsky, Vernon W.
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2018-11-05
Volume
19
Issue
11
Pages
3467
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms19113467
PMC
PMC6274918
OpenAlex
W2900236795
Cited by
128
References
93
Citations by year
2026: 13 · 2025: 21 · 2024: 16 · 2023: 13 · 2022: 21 · 2021: 21 · 2020: 19 · 2019: 4
FWCI
2.45
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Canadian Institutes of Health Research (136885)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › 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
gestational diabetes mellitus, insulin resistance in pregnancy, adipokines, lipotoxicity, inflammation, oxidative stress, beta-cell dysfunction, glucose homeostasis, hyperglycemia, therapeutic target
MeSH terms
Adaptation, Physiological, Female, Humans, Placenta, Pregnancy, Signal Transduction, Diabetes, Gestational, Oxidative Stress, Insulin-Secreting Cells

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