ArticleHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme2011
Prolactin activation of the long form of its cognate receptor causes increased visceral fat and obesity in males as shown in transgenic mice expressing only this receptor subtype.
Article in Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- From the perspective of prolactin: a view on obesity.Frontiers in endocrinology · 2026Review
- The Effect of Metformin on Pituitary Function in Postmenopausal Women with Subclinical Hypothyroidism and Macroprolactinemia: A Single-Center Prospective Case-Control Study.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Effects of Prolactin Inhibition on Lipid Metabolism in Goats.Animals : an open access journal from MDPI · 2024Article
- Hormonal Determinants of Growth and Weight Gain in the Human Fetus and Preterm Infant.Nutrients · 2023Review
- Characterization of anFrontiers in pharmacology · 2023Article
- Dopamine receptor agonists mechanism of actions on glucose lowering and their connections with prolactin actions.Frontiers in clinical diabetes and healthcare · 2023Review
- PRL/PRLR Can Promote Insulin Resistance by Activating the JAK2/STAT5 Signaling Pathway.Computational and mathematical methods in medicine · 2022Article
- Combined Anti-Adipogenic Effects of Hispidulin andBiomolecules · 2021Article
- Oxytocin and Vasopressin Systems in Obesity and Metabolic Health: Mechanisms and Perspectives.Current obesity reports · 2019Review
- The search for new biomarkers for cognition in schizophrenia.Schizophrenia research. Cognition · 2015Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
To date the best defined function of prolactin (PRL) is its action on the ovary and mammary gland, although it has also been shown to have an effect on lipid metabolism. Using mice engineered to express only the long form of the prolactin receptor (PRL-RL), we demonstrate that PRL acting through PRL-RL alone causes severe adipose accumulation in visceral fat of males at 6 months of age. The increase in visceral fat accumulation is attributed to loss of adipose-derived leptin, which results in diminished lipolysis. The reduction in leptin also corresponds to decreased activation of AMP-activated protein kinase (AMPK), which further results in diminished fatty acid oxidation and increased fatty acid synthesis. Interestingly, the blunted AMPK response was only observed in adipose tissue and not in liver suggesting that this PRL mediated effect is tissue specific. A glucose tolerance study inferred that PRL-RL mice may suffer from insulin resistance or a reduction in insulin production that is not due to aberrant expression of glucose transporter 4 (Glut4). Collectively, our findings demonstrate that PRL signaling through the long form receptor causes reduced fatty acid oxidation, increased lipid storage, glucose intolerance, and obesity. These findings are of great importance towards understanding the etiology of obesity associated with hyperprolactinemia in humans as well as the role of PRL as a metabolic regulator in adipose tissue.
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