In:
The Kaohsiung Journal of Medical Sciences, Wiley, Vol. 33, No. 5 ( 2017-05), p. 224-228
Abstract:
Glucose‐stimulated insulin secretion (GSIS) is one of the important physiological characteristics of islet β cells, and extracellular‐regulated protein kinase 1/2 (ERK1/2) is an important member of the mitogen‐activated protein kinase family that regulates this process. The inflammatory cytokine interleukin (IL)‐1β can inhibit the insulin secretion of pancreatic β cells, but the exact mechanism is unclear. This study was designed to investigate the inhibitory effect of IL‐1β on GSIS in βTC‐6 cells and its relation with the ERK1/2 signal transduction pathway. β‐TC6 cells were cultured and stimulated with 0mM, 1.38mM, or 5.5mM glucose. In addition, GSIS in β‐TC6 cells was blocked by IL‐1β at concentrations of 0.15 ng/mL, 1.5 ng/mL, and 15 ng/mL. After glucose stimulation and IL‐1β intervention, the insulin level in the cell supernatant was detected by radioimmunoassay, and the phosphorylation level of ERK1/2 was detected by western blotting assay. The insulin level in the 1.38mM glucose group was 108.52 ± 5.94 uIU/mL, which was significantly higher than the 0mM and 5.5mM glucose groups ( p 〈 0.05). Compared with the 0mM glucose group, the level of ERK1/2 phosphorylation was increased in the 1.38mM and 5.5mM glucose groups. After intervention by 0.15 ng/mL, 1.5 ng/mL, and 15 ng/mL IL‐1β, the level of ERK1/2 phosphorylation induced by 1.38mM glucose stimulation decreased in a dose‐dependent manner, and the insulin level correspondingly decreased. IL‐1β can inhibit GSIS in βTC‐6 cells, which is related to its inhibition of the phosphorylation of ERK1/2.
Type of Medium:
Online Resource
ISSN:
1607-551X
,
2410-8650
DOI:
10.1016/j.kjms.2017.02.006
Language:
English
Publisher:
Wiley
Publication Date:
2017
detail.hit.zdb_id:
2202782-8
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