ArticleFrontiers in endocrinology2021
Prolactin-Induced Adaptation in Glucose Homeostasis in Mouse Pregnancy Is Mediated by the Pancreas and Not in the Forebrain.
Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Prolactin receptor signalling contributes to the attenuation of stress-induced hyperthermia during pregnancy.Journal of neuroendocrinology · 2026Article
- Distinct macronutrient ratios optimize offspring survival, growth, and maternal glucose tolerance across mouse reproduction.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Unveiling Gestational Diabetes: An Overview of Pathophysiology and Management.International journal of molecular sciences · 2025Review
- Dopamine D2 receptor antagonist counteracts hyperglycemia and insulin resistance in diet-induced obese male mice.PloS one · 2024Article
- Astragalus polysaccharide promotes autophagy and alleviates diabetic nephropathy by targeting the lncRNA Gm41268/PRLR pathway.Renal failure · 2023Article
- Metabolic effects of prolactin and the role of dopamine agonists: A review.Frontiers in endocrinology · 2022Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
Adaptive changes in glucose homeostasis during pregnancy require proliferation of insulin-secreting beta-cells in the pancreas, together with increased sensitivity for glucose-stimulated insulin secretion. Increased concentrations of maternal prolactin/placental lactogen contribute to these changes, but the site of action remains uncertain. Use of Cre-lox technology has generated pancreas-specific prolactin receptor (Prlr) knockouts that demonstrate the development of a gestational diabetic like state. However, many Cre-lines for the pancreas also express Cre in the hypothalamus and prolactin could act centrally to modulate glucose homeostasis. The aim of the current study was to examine the relative contribution of prolactin action in the pancreas and brain to these pregnancy-induced adaptations in glucose regulation. Deletion of prolactin receptor (Prlr) from the pancreas using Pdx-cre or Rip-cre led to impaired glucose tolerance and increased non-fasting blood glucose levels during pregnancy. Prlr
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