An extremely low frequency magnetic field attenuates insulin secretion from the insulinoma cell line, RIN‐m

Sakurai, Tomonori; Satake, Akira; Sumi, Shoichiro; Inoue, Kazutomo; Miyakoshi, Junji

doi:10.1002/bem.10181

Cited by 37 publications

(25 citation statements)

References 26 publications

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“…Media then were removed and replaced again with 25 mM glucose. The cells were incubated for 16 h, and the insulin content was determined by ELISA (18).…”

Section: Construction Of Short Interfering Rnas (Sirnas) and Transfecmentioning

confidence: 99%

The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion

Harashima

Clark

Christie

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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IA-2 is an enzymatically inactive member of the transmembrane protein tyrosine phosphate family located in dense core secretory vesicles and a major autoantigen in type 1 diabetes. Recent studies showed that targeted disruption of the IA-2 gene in mice resulted in impairment of insulin secretion and glucose intolerance. Insulin homeostasis, however, is a complex process involving a cascade of regulatory factors, and IA-2 is widely expressed in neuroendocrine cells throughout the body. Consequently, it is uncertain whether the impairment of insulin secretion in IA-2 knockout mice is a direct result of the knockout of IA-2 in beta cells or to counter regulatory alterations resulting from IA-2 knockout in other neuroendocrine cells. To define the function of IA-2, we studied the secretion of insulin in a single cell type, MIN-6, by overexpressing and knocking down IA-2. Our experiments showed that overexpression of IA-2 resulted in a 6-fold increase in glucose-or K ؉ -induced insulin secretion and a Ϸ3-fold increase in the number of secretory vesicles and the insulin content of cells. In contrast, knockdown of endogenous IA-2 by short interfering RNA resulted in nearly a complete loss of glucose-induced insulin secretion and a 50% decrease in basal insulin release. The half-life of insulin in cells overexpressing IA-2 was nearly twice as great as that in mock-transfected cells, suggesting that IA-2 was stabilizing the insulin-containing vesicles. From these results we conclude that in beta cells, IA-2 is an important regulator of dense core vesicle number and glucoseinduced and basal insulin secretion.beta cells ͉ MIN-6 cells ͉ short interfering RNA ͉ glucose

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“…Media then were removed and replaced again with 25 mM glucose. The cells were incubated for 16 h, and the insulin content was determined by ELISA (18).…”

Section: Construction Of Short Interfering Rnas (Sirnas) and Transfecmentioning

confidence: 99%

The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion

Harashima

Clark

Christie

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…Most recently, we demonstrated that exposure to ELFMF for 1 or 2 h decreased insulin secretion in vitro [Sakurai et al, 2004[Sakurai et al, , 2005a. In normal rats, long-term exposure to ELFMF has been shown to lead to an increase in plasma insulin concentration [Laitl-Kobierska et al, 2002].…”

Section: Introductionmentioning

confidence: 98%

Exposure to extremely low frequency magnetic fields affects insulin‐secreting cells

Sakurai

Yoshimoto

Koyama

et al. 2007

Bioelectromagnetics

Self Cite

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To evaluate the effects of extremely low frequency magnetic field (ELFMF) on beta-cell survival and function, we cultured a hamster-derived insulin-secreting cell line (HIT-T15), which exhibits responsiveness to glucose in a semi-physiological range, under exposure to sham and ELFMF conditions, and assessed cell survival and function. We used our previously developed ELFMF exposure unit (a sinusoidal magnetic field at a frequency of 60 Hz, 5 mT) to culture cells under exposure to ELFMF conditions. We found that exposure to ELFMF for 5 days in the absence of glucose increased cell number, exposure for 2 days in the absence of glucose and for 5 days with 100 mg/dl glucose increased the insulin secretion to the culture medium, and exposure for 2 and 5 days with 40 and 100 mg/dl glucose increased intracellular insulin concentration in HIT-T15 cells. The increase in cell number under apoptotic culture conditions by exposure to ELFMF could lead to new therapeutic concepts in the treatment of diabetes. The ELFMF-induced increase in intracellular insulin concentration could be utilized to develop culture conditions to enhance intracellular insulin concentration in insulin-secreting cells that would be useful for cell transplantation to cure diabetes mellitus.

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“…There are many evidences supporting the hypoglycemic ability of magnetic field exposure, but the optimum frequency and exposure time remain unclear (17)(18)(19)(20)(21). Öcal et al (10) investigated the effect of 5mT and 8mT on healthy and diabetic rats for the duration of 165 minutes for three weeks.…”

Section: Discussionmentioning

confidence: 99%

Comparative and Mixture Effect of Cynodon Dactylon, ElectroMagnetic Field and Insulin on Diabetic Mouse

Nafisi¹,

Nezhady²,

Asghari³

2012

Balkan Med J

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An extremely low frequency magnetic field attenuates insulin secretion from the insulinoma cell line, RIN‐m

Cited by 37 publications

References 26 publications

The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion

The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion

Exposure to extremely low frequency magnetic fields affects insulin‐secreting cells

Comparative and Mixture Effect of Cynodon Dactylon, ElectroMagnetic Field and Insulin on Diabetic Mouse

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