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Normal Pregnancy-Induced Islet Beta Cell Proliferation in Mouse Models That Are Deficient in Serotonin-Signaling.

Lotte Goyvaerts¹, Anica Schraenen¹, Katleen Lemaire¹

¹Gene Expression Unit, Department of Cellular and Molecular Medicine, KU Leuven, 3000 Leuven, Belgium.

International Journal of Molecular Sciences

|December 23, 2022

Summary

Serotonin, produced by pancreatic islet beta cells during pregnancy, does not drive beta cell proliferation. Studies show that removing tryptophan hydroxylase 1 (Tph1) or 5-HT2B receptors did not affect this key pregnancy adaptation.

Keywords:

beta cell proliferation pregnancy serotonin

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Area of Science:

Endocrinology
Developmental Biology
Metabolic Research

Background:

Pregnancy involves hormonal changes, including placental lactogens stimulating pancreatic islet beta cells.
This stimulation upregulates tryptophan hydroxylase 1 (Tph1) expression, leading to serotonin synthesis in beta cells.
The functional role of this pregnancy-induced serotonin in beta cell adaptation remains largely unknown.

Purpose of the Study:

To investigate the hypothesis that serotonin signaling via 5-HT2B receptors promotes beta cell proliferation during mouse pregnancy.
To determine the necessity of islet serotonin production and 5-HT2B receptor signaling for pregnancy-induced beta cell expansion.

Main Methods:

Utilized three distinct mouse models: total Tph1 knockout (Tph1KO) mice, 129P2/OlaHsd mice with impaired islet Tph1 upregulation, and Htr2b-deficient mice lacking 5-HT2B receptors.
Assessed beta cell proliferation levels during pregnancy in these genetically modified mouse lines.
Compared proliferation rates against normal physiological responses observed in wild-type mice.

Main Results:

Normal pregnancy-induced beta cell proliferation was observed in total Tph1KO mice.
129P2/OlaHsd mice, despite altered islet Tph1 expression, exhibited normal beta cell proliferation.
Htr2b-deficient mice also showed no impairment in pregnancy-associated beta cell expansion.

Conclusions:

Islet serotonin production, mediated by Tph1, is not essential for the compensatory beta cell proliferation during mouse pregnancy.
Signaling through 5-HT2B receptors on beta cells is not required for this critical pregnancy-related adaptation.
These findings decouple the previously observed link between pregnancy-induced islet serotonin and beta cell expansion.