Normal Pregnancy-Induced Islet Beta Cell Proliferation in Mouse Models That Are Deficient in Serotonin-Signaling
During mouse pregnancy placental lactogens stimulate prolactin receptors on pancreatic islet beta cells to induce expression of the tryptophan hydroxylase <i>Tph1</i>, resulting in the synthesis and secretion of serotonin. Presently, the functional relevance of this phenomenon is unclear...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2022-12-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/23/24/15816 |
| Summary: | During mouse pregnancy placental lactogens stimulate prolactin receptors on pancreatic islet beta cells to induce expression of the tryptophan hydroxylase <i>Tph1</i>, resulting in the synthesis and secretion of serotonin. Presently, the functional relevance of this phenomenon is unclear. One hypothesis is that serotonin-induced activation of 5-HT<sub>2B</sub> receptors on beta cells stimulates beta cell proliferation during pregnancy. We tested this hypothesis via three different mouse models: (i) total <i>Tph1</i>KO mice, (ii) 129P2/OlaHsd mice, which are incompetent to upregulate islet <i>Tph1</i> during pregnancy, whereas <i>Tph1</i> is normally expressed in the intestine, mammary glands, and placenta, and (iii) <i>Htr2b</i>-deficient mice. We observed normal pregnancy-induced levels of beta cell proliferation in total <i>Tph1</i>KO mice, 129P2/OlaHsd mice, and in <i>Htr2b</i><sup>−/−</sup> mice. The three studied mouse models indicate that islet serotonin production and its signaling via 5-HT<sub>2B</sub> receptors are not required for the wave of beta cell proliferation that occurs during normal mouse pregnancy. |
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| ISSN: | 1661-6596 1422-0067 |