ArticleDiabetes2016
Gestational Diabetes Mellitus From Inactivation of Prolactin Receptor and MafB in Islet β-Cells.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- Prolactin in relation to gestational diabetes and metabolic risk in pregnancy and postpartum: A systematic review and meta-analysis.Frontiers in endocrinology · 2022Pooled it
- Sex Differences in ER Stress Pathways Are a Key Determinant of β-Cell Proliferation and Resilience.Diabetes · 2026Article
- Heat shock protein 72 (HSP72) modulates glucagon secretion via JNK inhibition in pancreatic α-cells.Diabetology international · 2026Article
- Advances and challenges in the mechanistic understanding of beta-cell dysfunction in gestational diabetes mellitus.Journal of animal science · 2026Review
- From the perspective of prolactin: a view on obesity.Frontiers in endocrinology · 2026Review
- Cell Type-Specific Hormonal Signaling Configures Hypothalamic Circuits for Parenting.bioRxiv : the preprint server for biology · 2025Article
- The human placenta and its role in reproductive outcomes revisited.Physiological reviews · 2025Review
- c-Jun regulates postpartum β-cell apoptosis and survival downstream of prolactin signaling.Molecular and cellular endocrinology · 2025Article
- A new paradigm of islet adaptations in human pregnancy: insights from immunohistochemistry and proteomics.Nature communications · 2025Article
- Mechanisms of Fetal Overgrowth in Gestational Diabetes: The Potential Role of SOCS2.Nutrients · 2025Review
- Unveiling Gestational Diabetes: An Overview of Pathophysiology and Management.International journal of molecular sciences · 2025Review
- Gestational Diabetes Mellitus: Mechanisms Underlying Maternal and Fetal Complications.Endocrinology and metabolism (Seoul, Korea) · 2025Review
- MAFB-mediated CEBPA regulated human urothelium growth through Wnt/β-catenin signaling pathway.Genes & diseases · 2025Article
- The beneficial and detrimental effects of prolactin hormone on metabolic syndrome: A double-edge sword.Journal of cellular and molecular medicine · 2024Review
- Prolactin: structure, receptors, and functions.Reviews in endocrine & metabolic disorders · 2024Review
- Diagnosis of hypoprolactinemia.Reviews in endocrine & metabolic disorders · 2024Review
- Pancreatic beta-cell mass and function and therapeutic implications of using antidiabetic medications in type 2 diabetes.Journal of diabetes investigation · 2024Review
- Acinar to β-like cell conversion through inhibition of focal adhesion kinase.Nature communications · 2024Article
- Impact of Ghrelin on Islet Size in Nonpregnant and Pregnant Female Mice.Endocrinology · 2024Article
- Kisspeptin upregulates β-cell serotonin production during pregnancy.The Journal of endocrinology · 2024Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.