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

ABSTRACT:

Objective

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, K⁺ flux through endoplasmic reticulum (ER)-localized TALK-1 channels enhances ER Ca²⁺ leak, modulating Ca²⁺ handling and insulin secretion. As glucose amplification of islet somatostatin release relies on Ca²⁺-induced Ca²⁺ release (CICR) from the δ-cell ER, we investigated whether TALK-1 modulates δ-cell Ca²⁺ handling and somatostatin secretion.

Methods

To define the functions of islet δ-cell TALK-1

SUBMITTER: Vierra NC 

PROVIDER: S-EPMC5870147 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature