Stimulus-secretion coupling of hypotonicity-induced insulin release in BRIN-BD11 cells

Beauwens, R; Best, Len; Markadieu, N; Crutzen, R; Louchami, K; Brown, P; Yates, AP; Malaisse, WJ; Sener, A

HERO ID

2791674

Reference Type

Journal Article

Year

2006

Language

English

PMID

17526948

HERO ID 2791674
In Press No
Year 2006
Title Stimulus-secretion coupling of hypotonicity-induced insulin release in BRIN-BD11 cells
Authors Beauwens, R; Best, Len; Markadieu, N; Crutzen, R; Louchami, K; Brown, P; Yates, AP; Malaisse, WJ; Sener, A
Journal Endocrine
Volume 30
Issue 3
Page Numbers 353-363
Abstract The stimulus-secretion coupling for hypotonicity-induced insulin release was investigated in BRIN-BD11 cells. A 50 mM decrease in extracellular NaCl caused a twofold increase in insulin release. The release of insulin evoked by hypotonicity progressively decreased in an exponential manner. The response to extracellular hypotonicity displayed a threshold value close to 20 mOsmol/L and a maximal response at about 70 mOsmol/ L. Hypotonicity also caused a rapid increase in cell volume followed by a regulatory volume decrease (RVD), cell membrane depolarization with induction of spike activity, and a rise in cytosolic Ca2+ concentration. 5-Nitro-2-(3-phenylpropylamino)benzoate inhibited the secretory response to hypoosmolarity, failed to affect the early increase in cell volume but prevented the RVD, and suppressed the hypotonicity-induced plasma membrane depolarization. Insulin release provoked by hypotonicity was inhibited by verapamil, absence of Ca2+, thapsigargin, furosemide, tributyltin, and diazoxide. On the contrary, tolbutamide augmented modestly insulin release recorded in the hypoosmolar medium. Last, a rise in extracellular K+ concentration, while augmenting basal insulin output, failed to affect insulin release in the hypoosmolar medium. Thus, the insulin secretory response to hypotonicity apparently represents a Ca2+-dependent process triggered by the gating of volume-sensitive anion channels with subsequent depolarization and gating of voltage-sensitive Ca2+ channels.
Doi 10.1007/s12020-006-0014-3
Pmid 17526948
Wosid WOS:000246018300014
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword hypotonicity; insulin release; BRIN-BD11 cells