Pancreatic GABA and Serotonin Actions in the Pancreas and Fetal Programming of Metabolism

Hill, David J.

doi:10.1007/978-3-319-60289-9_38

Cited by 2 publications

(1 citation statement)

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“…Serotonin levels are triggering insulin secretion and β-cell proliferation. 53 Serotonin is also reported to be produced in β-cells to inhibit α-cell glucagon expression (however, we did not find striking evidence of glucagon lower levels in 3D biochips). Furthermore, without serotonin, the regulation of glucagon in α-cells is unpaired during the islets’ response to glucose stimulation.…”

Section: Discussioncontrasting

confidence: 63%

Analysis of the transcriptome and metabolome of pancreatic spheroids derived from human induced pluripotent stem cells and matured in an organ-on-a-chip

et al. 2022

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Section: Discussioncontrasting

confidence: 63%

Analysis of the transcriptome and metabolome of pancreatic spheroids derived from human induced pluripotent stem cells and matured in an organ-on-a-chip

et al. 2022

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Life‐long impairment of glucose homeostasis upon prenatal exposure to psychostimulants

et al. 2019

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Maternal drug abuse during pregnancy is a rapidly escalating societal problem. Psychostimulants, including amphetamine, cocaine, and methamphetamine, are amongst the illicit drugs most commonly consumed by pregnant women. Neuropharmacology concepts posit that psychostimulants affect monoamine signaling in the nervous system by their affinities to neurotransmitter reuptake and vesicular transporters to heighten neurotransmitter availability extracellularly. Exacerbated dopamine signaling is particularly considered as a key determinant of psychostimulant action. Much less is known about possible adverse effects of these drugs on peripheral organs, and if in utero exposure induces lifelong pathologies. Here, we addressed this question by combining human RNA‐seq data with cellular and mouse models of neuroendocrine development. We show that episodic maternal exposure to psychostimulants during pregnancy coincident with the intrauterine specification of pancreatic β cells permanently impairs their ability of insulin production, leading to glucose intolerance in adult female but not male offspring. We link psychostimulant action specifically to serotonin signaling and implicate the sex‐specific epigenetic reprogramming of serotonin‐related gene regulatory networks upstream from the transcription factor Pet1/Fev as determinants of reduced insulin production.

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Pancreatic GABA and Serotonin Actions in the Pancreas and Fetal Programming of Metabolism

Cited by 2 publications

References 83 publications

Analysis of the transcriptome and metabolome of pancreatic spheroids derived from human induced pluripotent stem cells and matured in an organ-on-a-chip

Analysis of the transcriptome and metabolome of pancreatic spheroids derived from human induced pluripotent stem cells and matured in an organ-on-a-chip

Life‐long impairment of glucose homeostasis upon prenatal exposure to psychostimulants

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