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Horm Metab Res 2001; 33(5): 281-289
DOI: 10.1055/s-2001-15284
Original Clinical
© Georg Thieme Verlag Stuttgart · New York

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

E. Adeghate1 , A. S. Ponery1 , A. Wahab2
  • 1 Dept. of Human Anatomy, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates
  • 2 Dept. of Medical Education, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates
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Publication History

Publication Date:
31 December 2001 (online)

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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 - 20 Hz, 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 α- and β-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.

Key words:

EFS - Insulin - Glucagon - Pancreas - Diabetes Mellitus - Radioimmunoassay - TTX - Atropine - Propranolol - Yohimbine

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Dr. E. Adeghate

Department of Human Anatomy
Faculty of Medicine & Health Sciences
United Arab Emirates University

P.O. Box 17666
Al Ain
United Arab Emirates


Fax: Fax:+ 971 (3) 7672033

Email: E-mail:eadeghate@uaeu.ac.ae

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