Cited by 46Pancreatic function and diabetesDiabetes and associated disordersGrowth Hormone and Insulin-like Growth Factors

Defective prolactin signaling impairs pancreatic β-cell development during the perinatal period

Open access
Auffret, Julien, Freemark, Michael, Carré, Nadège, Mathieu, Yves, Tourrel-Cuzin, Cécile, Lombès, Marc, Movassat, Jamileh, Binart, Nadine·2013·American Journal of Physiology-Endocrinology and Metabolism

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.

Integrity signals

Registry

Crossref · 10.1152/ajpendo.00636.2012

Cites

47 of 47 references verified0 citation errors · 0 not checkable

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  • Prolactin is essential for adequate β-cell proliferation, as demonstrated in mouse knockouts of the prolactin receptor.

    “Prolactin is also essential for adequate β-cell proliferation, as demonstrated in mouse knockouts of the prolactin receptor (PrlR−/−) [80].”

    From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [80]

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1 of the 48 references couldn’t be matched to a known paper.

Research works printed but not linked: 3

  1. Freemark M, 1997, Implications for tissue differentiation and development. J Clin Invest, 99, 1107
  2. 10.1210/endo.133.4.8404626 · DOI
  3. 10.1172/jci0214439 · DOI

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Authors
Auffret, J., Freemark, M., Carré, N., Mathieu, Y., Tourrel-Cuzin, C., Lombès, M., Movassat, J., & Binart, N.
Affiliations
  • Université Paris-Sud (FR)
  • Duke University (US)
  • Centre National de la Recherche Scientifique (FR)
  • Université Paris Diderot, Sorbonne Paris Cité, CNRS EAC 4413, Équipe Biologie et Pathologie du Pancréas Endocrine, Paris, France; and
Corresponding author
Binart, Nadine
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2013-11-15
Volume
305
Issue
10
Pages
E1309-E1318
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2044428487
Cited by
46
References
48
Citations by year
2024: 8 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 8 · 2018: 3 · 2017: 2 · 2016: 8 · 2015: 4 · 2014: 4
FWCI
5.25
Type
journal article
Language
en
Open access
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Agence Nationale de la Recherche (ANR-09-BLAN-0246)
  • Institut National de la Santé et de la Recherche Médicale
  • Université Paris-Sud
  • National Institutes of Health
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
Keywords
prolactin signaling, prolactin receptor, pancreatic beta-cell development, beta-cell proliferation, perinatal period, mTOR signaling, insulin-like growth factor II, placental lactogen, type 2 diabetes, Goto-Kakizaki rats, embryonic pancreas
MeSH terms
Animals, Animals, Newborn, Cell Differentiation, Cells, Cultured, Embryo, Mammalian, Female, Pancreas, Pregnancy, Prolactin, Receptors, Prolactin, Signal Transduction, Rats, Wistar, Mice, Knockout, Insulin-Secreting Cells, Mice, Rats

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