Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

Priming of insulin granules for exocytosis by granular Cl(-) uptake and acidification

In English

Författare

Summary, in English

ATP-dependent priming of the secretory granules precedes Ca(2+)-regulated neuroendocrine secretion, but the exact nature of this reaction is not fully established in all secretory cell types. We have further investigated this reaction in the insulin-secreting pancreatic B-cell and demonstrate that granular acidification driven by a V-type H(+)-ATPase in the granular membrane is a decisive step in priming. This requires simultaneous Cl(-) uptake through granular ClC-3 Cl(-) channels. Accordingly, granule acidification and priming are inhibited by agents that prevent transgranular Cl(-) fluxes, such as 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and an antibody against the ClC-3 channels, but accelerated by increases in the intracellular ATP:ADP ratio or addition of hypoglycemic sulfonylureas. We suggest that this might represent an important mechanism for metabolic regulation of Ca(2+)-dependent exocytosis that is also likely to be operational in other secretory cell types.

Avdelning/ar

Publiceringsår

2001

Språk

Engelska

Sidor

2145-2154

Publikation/Tidskrift/Serie

Journal of Cell Science

Volym

114

Issue

Pt 11

Dokumenttyp

Artikel i tidskrift

Förlag

The Company of Biologists Ltd

Ämne

  • Endocrinology and Diabetes

Nyckelord

  • ClC-3 channels
  • Exocytosis
  • Sulfonylureas
  • Insulin
  • Granular pH

Status

Published

Forskningsgrupp

  • Islet cell physiology
  • Diabetes - Islet Cell Exocytosis
  • Diabetes - Islet Patophysiology

ISBN/ISSN/Övrigt

  • ISSN: 0021-9533