Adenosine triphosphate is co-secreted with glucagon-like peptide-1 to modulate intestinal enterocytes and afferent neurons

Lu Van B., Juraj Rievaj, Elisabeth A. O’Flaherty, Christopher A. Smith, Ramona Pais, Luke A. Pattison, Gwen Tolhurst, Andrew B. Leiter, David C. Bulmer, Fiona M. Gribble () and Frank Reimann ()
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Lu Van B.: University of Cambridge, Addenbrooke’s Hospital
Juraj Rievaj: University of Cambridge, Addenbrooke’s Hospital
Elisabeth A. O’Flaherty: University of Cambridge, Addenbrooke’s Hospital
Christopher A. Smith: University of Cambridge, Addenbrooke’s Hospital
Ramona Pais: University of Cambridge, Addenbrooke’s Hospital
Luke A. Pattison: University of Cambridge
Gwen Tolhurst: University of Cambridge, Addenbrooke’s Hospital
Andrew B. Leiter: University of Massachusetts Medical School
David C. Bulmer: University of Cambridge
Fiona M. Gribble: University of Cambridge, Addenbrooke’s Hospital
Frank Reimann: University of Cambridge, Addenbrooke’s Hospital

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Enteroendocrine cells are specialised sensory cells located in the intestinal epithelium and generate signals in response to food ingestion. Whilst traditionally considered hormone-producing cells, there is evidence that they also initiate activity in the afferent vagus nerve and thereby signal directly to the brainstem. We investigate whether enteroendocrine L-cells, well known for their production of the incretin hormone glucagon-like peptide-1 (GLP-1), also release other neuro-transmitters/modulators. We demonstrate regulated ATP release by ATP measurements in cell supernatants and by using sniffer patches that generate electrical currents upon ATP exposure. Employing purinergic receptor antagonists, we demonstrate that evoked ATP release from L-cells triggers electrical responses in neighbouring enterocytes through P2Y2 and nodose ganglion neurones in co-cultures through P2X2/3-receptors. We conclude that L-cells co-secrete ATP together with GLP-1 and PYY, and that ATP acts as an additional signal triggering vagal activation and potentially synergising with the actions of locally elevated peptide hormone concentrations.

Date: 2019
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DOI: 10.1038/s41467-019-09045-9

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