ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Defective prolactin signaling impairs pancreatic β-cell development during the perinatal period.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Comparison of tumour and serum specific microRNA changes dissecting their role in pancreatic ductal adenocarcinoma: a meta-analysis.BMC cancer · 2019Pooled it
- Cell size regulates human endoderm specification through actomyosin-dependent AMOT-YAP signaling.Stem cell reports · 2024Article
- Investigating the Role of 17-Beta Estradiol in the Regulation of the Unfolded Protein Response (UPR) in Pancreatic Beta Cells.International journal of molecular sciences · 2024Article
- Dopamine D2 receptor antagonist counteracts hyperglycemia and insulin resistance in diet-induced obese male mice.PloS one · 2024Article
- Metformin in Gestational Diabetes Mellitus: To Use or Not to Use, That Is the Question.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Immunomodulatory role of decidual prolactin on the human fetal membranes and placenta.Frontiers in immunology · 2023Review
- Review
- The beneficial metabolic actions of prolactin.Frontiers in endocrinology · 2022Review
- Beta cell adaptation to pregnancy requires prolactin action on both beta and non-beta cells.Scientific reports · 2021Article
- Prolactin Is Associated With Insulin Resistance and Beta-Cell Dysfunction in Infertile Women With Polycystic Ovary Syndrome.Frontiers in endocrinology · 2021Observational
- Murine Perinatal β-Cell Proliferation and the Differentiation of Human Stem Cell-Derived Insulin-Expressing Cells Require NEUROD1.Diabetes · 2019Article
- Prolactin - a pleiotropic factor in health and disease.Nature reviews. Endocrinology · 2019Review
- Co-shared genetics and possible risk gene pathway partially explain the comorbidity of schizophrenia, major depressive disorder, type 2 diabetes, and metabolic syndrome.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019Review
- The Pathophysiology of Gestational Diabetes Mellitus.International journal of molecular sciences · 2018Review
- Synaptotagmin 4 Regulates Pancreatic β Cell Maturation by Modulating the CaDevelopmental cell · 2018Article
- Characterization of the Molecular Mechanisms Underlying Glucose Stimulated Insulin Secretion from Isolated Pancreatic β-cells Using Post-translational Modification Specific Proteomics (PTMomics).Molecular & cellular proteomics : MCP · 2018Article
- Gestational Diabetes Mellitus From Inactivation of Prolactin Receptor and MafB in Islet β-Cells.Diabetes · 2016Article
- Dopamine-prolactin pathway potentially contributes to the schizophrenia and type 2 diabetes comorbidity.Translational psychiatry · 2016Review
- Pancreatic β Cell Mass Death.Frontiers in pharmacology · 2016Review
- Cell biology. On being the right (cell) size.Science (New York, N.Y.) · 2015Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prolactin (PRL) and placental lactogens stimulate β-cell replication and insulin production in pancreatic islets and insulinoma cells through binding to the PRL receptor (PRLR). However, the contribution of PRLR signaling to β-cell ontogeny and function in perinatal life and the effects of the lactogens on adaptive islet growth are poorly understood. We provide evidence that expansion of β-cell mass during both embryogenesis and the postnatal period is impaired in the PRLR(-/-) mouse model. PRLR(-/-) newborns display a 30% reduction of β-cell mass, consistent with reduced proliferation index at E18.5. PRL stimulates leucine incorporation and S6 kinase phosphorylation in INS-1 cells, supporting a role for β-cell mTOR signaling in PRL action. Interestingly, a defect in the development of acini is also observed in absence of PRLR signaling, with a sharp decline in cellular size in both endocrine and exocrine compartments. Of note, a decrease in levels of IGF-II, a PRL target, in the Goto-Kakizaki (GK) rat, a spontaneous model of type 2 diabetes, is associated with a lack of PRL-mediated β-cell proliferation in embryonic pancreatic buds. Reduced pancreatic IGF-II expression in both rat and mouse models suggests that this factor may constitute a molecular link between PRL signaling and cell ontogenesis. Together, these results provide evidence that PRL signaling is essential for pancreas ontogenesis during the critical perinatal window responsible for establishing functional β-cell reserve.
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