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

Tomonori Sakurai1, Akira Satake, Shoichiro Sumi

  • 1Department of Organ Reconstruction, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan.

Bioelectromagnetics
|March 26, 2004
PubMed

Insights

Extremely low frequency magnetic fields (ELFMF) significantly reduce insulin secretion from pancreatic cells. This effect is linked to reduced calcium influx and altered gene expression, suggesting ELFMF impacts hormone release mechanisms.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Biophysics

Background:

  • Hormone secretion, particularly insulin, is crucial for metabolic regulation.
  • Extremely low frequency magnetic fields (ELFMF) are ubiquitous, and their biological effects warrant investigation.
  • Pancreatic beta-cells are responsible for insulin production and secretion.

Purpose of the Study:

  • To investigate the impact of ELFMF exposure on insulin secretion from an insulinoma cell line (RIN-m).
  • To elucidate the underlying mechanisms of ELFMF-induced changes in insulin release.

Main Methods:

  • RIN-m cells were exposed to a 5 mT, 60 Hz ELFMF or sham conditions for 1 hour.
  • Insulin secretion was stimulated using 45 mM KCl.
  • Effects of nifedipine on insulin secretion were assessed.
  • mRNA expression of SNAP-25 and synaptotagmin 1 was analyzed.

Main Results:

  • ELFMF exposure significantly attenuated insulin release compared to sham exposure.
  • Nifedipine treatment partially reversed the inhibitory effect of ELFMF on insulin secretion.
  • ELFMF exposure decreased the mRNA expression of SNAP-25 and synaptotagmin 1.

Conclusions:

  • ELFMF exposure attenuates insulin secretion from RIN-m cells.
  • The mechanism involves impaired calcium influx through calcium channels.
  • ELFMF affects key proteins involved in exocytosis and calcium signaling.

Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...