Effect of Electrical Field Stimulation on Insulin and Glucagon Secretion from the Pancreas of Normal and Diabetic Rats

Abstract

The effect of electrical field stimulation (EFS) on insulin (INS) and glucagon (GLU) secretion from normal and diabetic rat pancreas is poorly understood. In our study, EFS (5-20Hz, 50 V amplitude and 1.0 ms pulse width), when applied alone, resulted in a significant (p<0.05) increase in INS secretion from the pancreas of both normal and diabetic rats. Atropine (10(-5) M) did not inhibit the EFS (5 Hz)-evoked INS secretion in normal pancreas and failed to alter the effect of EFS (10-20 Hz) on INS secretion from the pancreas of both normal and diabetic rats. Propranolol (Prop) inhibited INS secretion to below basal level in the presence of EFS (5 Hz) but not at EFS (10- 20 Hz). Tetrodotoxin (TTX) also significantly (p = 0.002) inhibited INS secretion from normal pancreas in the presence of EFS (5-20 Hz). The decrease in insulin secretion observed when pancreatic tissue fragments were incubated in Prop and TTX in the presence of EFS was reversed by yohimbine (10(-5) M). In contrast, TTX did not significantly modify INS secretion from diabetic pancreas in the presence of EFS. EFS (5-20 Hz) significantly (p<0.05) increased GLU release from normal and diabetic rat pancreas when applied alone. Neither atropine, Prop nor TTX significantly modified GLU release from the pancreas of either normal or diabetic rats. This suggests that GLU secretion may be controlled through a different pathway. The EFS-evoked INS and GLU secretion is probably executed via different mechanisms. These mechanisms include 1) activation of cholinergic nerves by EFS; 2) EFS of alpha- and beta-adrenergic nerves; 3) activation of non-adrenergic non-cholinergic pathway by EFS; 4) EFS-induced depolarization and subsequent action potential in pancreatic endocrine cells and 5) electroporosity caused by EFS-induced membrane permeability. All of these effects may be summative. In conclusion, EFS (5-20 Hz), when applied alone, can evoke significant increases in INS and GLU secretion from the pancreas of both normal and diabetic rats. Insulin secretion is controlled via alpha-2 adrenergic (inhibition) and beta-adrenergic (stimulation) receptors. Glucagon secretion is enhanced by alpha2 adrenergic stimulation.

Role of Insulin/Glucagon Ratio and Cell Redox State in the Hyperglycaemia Induced by Exposure to Electromagnetic Fields in Rats.

“…The extremely low-frequency EMFs can affect Ca2 + mobilization and signaling, which can be involved in insulin release, and it has been found that 60-Hz EMFs stimulation increases insulin secretion in diabetic and normal rats [28,29]. Indeed, it has been shown that EMFs with the same frequency of the natural frequencies of β-cell increase insulin secretion, which may indicate strong energy (ATP) coupling between insulin secretion and EMFs [23].…”

The Role of Insulin/glucagon Ratio and Cell Redox State in the&nbsp;Hyperglycemia Induced by Exposure to Pulsed Electromagnetic Fields in Rats

“…The extremely low-frequency EMFs can affect Ca2 + mobilization and signaling, which can be involved in insulin release, and it has been found that 60-Hz EMFs stimulation increases insulin secretion in diabetic and normal rats (34,35). Indeed, it has been shown that EMFs with the same frequency of the natural frequencies of β-cell increase insulin secretion, which may indicate strong energy (ATP) coupling between insulin secretion and EMFs (29).…”

Neuromodulation of metabolic functions: from pharmaceuticals to bioelectronics to biocircuits

“…This process coordinates the release of insulin to achieve an effective regulation of glycolysis required to maintain glucose homeostasis. Electrical stimulation of pancreatic tissues induces the release of insulin [1]. β-cell activity is also regulated by direct neural innervation.…”