[Effects of iodine excess on islet β cells(β-TC-6) function and the mechanism].

Abstract

OBJECTIVE:

To explore the influences of iodine excess on insulin secret function of mouse insulinoma cells β-TC-6 and the mechanism.

METHODS:

β-TC-6 cells were treated with excessive iodine( Na I) in vitro. After 24 hour of exposure, the MTT assay was used to measure the cell viabilities. β-TC-6 cells, after 24 hour of exposure in excessive iodine, were stimulated with Krebs-Ringer bicarbonate buffer containing 5. 6mmol/L glucose for 1 hour at 37 ℃, then the supernatant was collected for insulin determination by ELISA kit. Western blot was used to detect the expression of Bcl-2, Bax, GRP78 and IRE1α.

RESULTS:

The rate of cell viability decreased from 1 mmol/L to 100mmol/L iodine excess group by a dose-dependent manner and was significantly lower than the control group and as follow by 73. 3%, 71. 2% and 55. 8% of that of control group. Iodine excess impaired the insulin secret function of β-TC-6 cells in 1 mmol/L and 100 mmol/L iodine excess groups. The expression of Bcl-2 decreased while the expressionof Bax increased significantly when compared with control group( P < 0. 05). From 1mmol/L iodine excess group, the expression of GRP78 and IRE1α were increased significantly when compared with control group( P < 0. 05).

CONCLUSION:

Iodine excess decreased the cell viabilities and impaired insulin secret function, which might be related to endoplasmic reticulum stress and Bcl-2 families.

• Authors: Zuolong Sun, Xiao Wang, Jin Chen, Peng Duan, Jing Wang, Ying Liu, Huailan Guo
• Journal: Wei sheng yan jiu = Journal of hygiene research (Wei Sheng Yan Jiu) Vol. 46 Issue 4 Pg. 610-614 (Jul 2017) ISSN: 1000-8020 [Print] China
• PMID: 29903184 (Publication Type: Journal Article)

Chemical References

• Endoplasmic Reticulum Chaperone BiP
• Hspa5 protein, mouse
• Insulin
• Iodides
• Iodine

Topics

• Animals
• Apoptosis
• Endoplasmic Reticulum Chaperone BiP
• Insulin
• Insulin-Secreting Cells (drug effects)
• Iodides
• Iodine (pharmacology)
• Mice