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Molecular Physiology & Biophysics

TALK-1 reduces delta-cell endoplasmic reticulum and cytoplasmic calcium levels limiting somatostatin secretion.

AUTHORS

Vierra NC , Dickerson MT , Jordan KL , Dadi PK , Kadare KA , Altman MK , Milian SC , Jacobson DA , . Molecular metabolism. 2018 3 ; 9(). 84-97

ABSTRACT

Single-cell RNA sequencing studies have revealed that the type-2 diabetes associated two-pore domain K(K2P) channel TALK-1 is abundantly expressed in somatostatin-secreting δ-cells. However, a physiological role for TALK-1 in δ-cells remains unknown. We previously determined that in β-cells, Kflux through endoplasmic reticulum (ER)-localized TALK-1 channels enhances ER Caleak, modulating Cahandling and insulin secretion. As glucose amplification of islet somatostatin release relies on Ca-induced Carelease (CICR) from the δ-cell ER, we investigated whether TALK-1 modulates δ-cell Cahandling and somatostatin secretion.

Single-cell RNA sequencing studies have revealed that the type-2 diabetes associated two-pore domain K(K2P) channel TALK-1 is abundantly expressed in somatostatin-secreting δ-cells. However, a physiological role for TALK-1 in δ-cells remains unknown. We previously determined that in β-cells, Kflux through endoplasmic reticulum (ER)-localized TALK-1 channels enhances ER Caleak, modulating Cahandling and insulin secretion. As glucose amplification of islet somatostatin release relies on Ca-induced Carelease (CICR) from the δ-cell ER, we investigated whether TALK-1 modulates δ-cell Cahandling and somatostatin secretion.

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