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Cited by 275Pancreatic function and diabetesGrowth Hormone and Insulin-like Growth FactorsGestational Diabetes Research and Management

Prolactin Receptor Is Required for Normal Glucose Homeostasis and Modulation of β-Cell Mass during Pregnancy

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Huang, Carol, Snider, Frances, Cross, James C.·2009·Endocrinology
DOI 10.1210/en.2008-1003
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Abstract

Increased islet mass is an adaptive mechanism that occurs to combat insulin resistance during pregnancy. Prolactin (PRL) can enhance β-cell proliferation and insulin secretion in vitro, yet whether it is PRL or other pregnancy-related factors that mediate these adaptive changes during pregnancy is unknown. The objective of this study was to determine whether prolactin receptor (Prlr) is required for normal maternal glucose homeostasis during pregnancy. An ip glucose tolerance test was performed on timed-pregnant Prlr+/+ and heterozygous null Prlr+/− mice on d 0, 15, and 18 of pregnancy. Compared with Prlr+/+ mice, Prlr+/− mice had impaired glucose clearance, decreased glucose-stimulated insulin release, higher nonfasted blood glucose, and lower insulin levels during but not before pregnancy. There was no difference in their insulin tolerance. Prlr+/+ mice show a significant incremental increase in islet density and β-cell number and mass throughout pregnancy, which was attenuated in the Prlr+/− mice. Prlr+/+ mice also had a more robust β-cell proliferation rate during pregnancy, whereas there was no difference in apoptosis rate between the Prlr+/+ and Prlr+/− mice before, during, or after pregnancy. Interestingly, genotype of the mothers had a significant impact on the offspring’s phenotype, such that daughters derived from Prlr+/− mothers had a more severe phenotype than those derived from Prlr+/+ mothers. In conclusion, this is the first in vivo demonstration that the action of pregnancy hormones, acting through Prlr, is required for normal maternal glucose tolerance during pregnancy by increasing β-cell mass.

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  • Pregnant mice heterozygous for the prolactin receptor null mutation show reduced β-cell proliferation, decreased β-cell size and mass, and impaired glucose tolerance.

    “The requirement of the prolactin receptor for β-cell adaptation during pregnancy was demonstrated using pregnant mice heterozygous for the prolactin receptor null mutation. These mice exhibited reduced β-cell proliferation, decreased β-cell size and mass, and impaired glucose tolerance [46].”

    From Expansion of β-cell mass in response to pregnancy (2010) · cites this paper as [46]

  • The maternal genotype significantly affects the phenotype of female offspring that become pregnant, as assessed by serum glucose levels.

    “Interestingly, the maternal genotype had a significant effect on the phenotype of female offspring that became pregnant, as assessed by serum glucose levels [46], suggesting that in utero exposure to impaired glucose homeostasis alters the epigenetic memory of β-cells [47–49].”

    From Expansion of β-cell mass in response to pregnancy (2010) · cites this paper as [46]

  • Cish and Socs2 act as negative regulators of tyrosine kinases and receptors that affect β-cell proliferation, including the prolactin receptor.

    “Each acts as a negative regulator of a variety of tyrosine kinases and receptors affecting β-cell proliferation, including the prolactin receptor [46].”

    From Expansion of β-cell mass in response to pregnancy (2010) · cites this paper as [46]

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Authors
Huang, C., Snider, F., & Cross, J. C.
Affiliations
University of Calgary (CA)
Corresponding author
Huang, Carol
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2008-11-26
Volume
150
Issue
4
Pages
1618-1626
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2008-1003
OpenAlex
W2148486284
Cited by
275
References
30
Citations by year
2026: 7 · 2025: 9 · 2024: 13 · 2023: 11 · 2022: 21 · 2021: 16 · 2020: 29 · 2019: 22 · 2018: 19 · 2017: 17 · 2016: 24 · 2015: 15 · 2014: 17 · 2013: 13 · 2012: 8
FWCI
11.97
Type
journal article
Language
en
Open access
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • Libraries and Cultural Resources (University of Calgary)
Funders
  • Children's Hospital Foundation
  • Alberta Children's Hospital Foundation
  • Canadian Institutes of Health Research (37776)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
prolactin receptor, prolactin, glucose homeostasis, beta-cell mass, beta-cell proliferation, pregnancy, glucose tolerance, insulin secretion, maternal glucose tolerance, transgenerational effects, insulin resistance
MeSH terms
Animals, Female, Genotype, Glucose, Glucose Tolerance Test, Homeostasis, Immunohistochemistry, Islets of Langerhans, Mice, Mutant Strains, Pregnancy, Receptors, Prolactin, Apoptosis, Glucose Intolerance, Cell Proliferation, Insulin-Secreting Cells, Mice

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