Gestational Diabetes Mellitus From Inactivation of Prolactin Receptor and MafB in Islet β-Cells
Open accessAbstract
β-Cell proliferation and expansion during pregnancy are crucial for maintaining euglycemia in response to increased metabolic demands placed on the mother. Prolactin and placental lactogen signal through the prolactin receptor (PRLR) and contribute to adaptive β-cell responses in pregnancy; however, the in vivo requirement for PRLR signaling specifically in maternal β-cell adaptations remains unknown. We generated a floxed allele of Prlr, allowing conditional loss of PRLR in β-cells. In this study, we show that loss of PRLR signaling in β-cells results in gestational diabetes mellitus (GDM), reduced β-cell proliferation, and failure to expand β-cell mass during pregnancy. Targeted PRLR loss in maternal β-cells in vivo impaired expression of the transcription factor Foxm1, both G1/S and G2/M cyclins, tryptophan hydroxylase 1 (Tph1), and islet serotonin production, for which synthesis requires Tph1. This conditional system also revealed that PRLR signaling is required for the transient gestational expression of the transcription factor MafB within a subset of β-cells during pregnancy. MafB deletion in maternal β-cells also produced GDM, with inadequate β-cell expansion accompanied by failure to induce PRLR-dependent target genes regulating β-cell proliferation. These results unveil molecular roles for PRLR signaling in orchestrating the physiologic expansion of maternal β-cells during pregnancy.
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Prolactin regulates β-cell adaptation against increased insulin resistance during pregnancy.
“Prolactin, a hormone secreted from the pituitary during pregnancy and lactation, regulates β-cell adaptation against increased insulin resistance during pregnancy [79].”
From Gestational Diabetes Mellitus: Diagnostic Approaches and Maternal-Offspring Complications (2022) · cites this paper as [79]
The Introduction says pregnancy increases the demand for insulin and that prolactin signals through a receptor involved in β-cell adaptation. The paper also reports that loss of this receptor impairs β-cell expansion during pregnancy. It does not specifically attribute that demand to increased insulin resistance or establish the cited sentence’s claim about prolactin’s pituitary origin. (LLM, conf=0.83)
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Self-citation
- Authors
- Banerjee, R. R., Cyphert, H. A., Walker, E. M., Chakravarthy, H., Peiris, H., Gu, X., Liu, Y., Conrad, E., Goodrich, L., Stein, R. W., & Kim, S. K.
- Affiliations
- Stanford Medicine (US)
- Vanderbilt University (US)
- Harvard University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Kim, Seung K.
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2016-05-23
- Volume
- 65
- Issue
- 8
- Pages
- 2331-2341
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC4955982
- OpenAlex
- W2407055585
- Semantic Scholar
- 1d3a6119900285beed9f6c6b35e67c75d0d223f0
- Cited by
- 131
- References
- 50
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 17 · 2023: 17 · 2022: 14 · 2021: 11 · 2020: 19 · 2019: 14 · 2018: 12 · 2017: 8
- FWCI
- 12.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Diabetes (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (K-08 DK091359, DK-090570, DK-089572, DK-050203)
- National Institutes of Health (1F-32 DK-102283)
- JDRF
- American Diabetes Association (1-16-PDF-086)
- Snyder Foundation
- Helmsley Trust
- Howard Hughes Medical Institute
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- gestational diabetes mellitus, prolactin receptor, MAFB, pancreatic beta-cell proliferation, beta-cell mass expansion, pregnancy, placental lactogen, FOXM1, tryptophan hydroxylase 1, conditional gene deletion, cyclins
- MeSH terms
- Forkhead Box Protein M1, Animals, Cells, Cultured, Female, Insulin, Male, Mice, Inbred C57BL, Pregnancy, Receptors, Prolactin, Serotonin, Tryptophan Hydroxylase, Signal Transduction, Diabetes, Gestational, Mice, Knockout, Cyclin D1, Cell Proliferation, Insulin-Secreting Cells, MafB Transcription Factor, Mice, Cyclin D2, Cyclin B1, Cyclin A2, Cyclin B2
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