Letter to the Editor Open Access
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Mar 26, 2024; 12(9): 1712-1713
Published online Mar 26, 2024. doi: 10.12998/wjcc.v12.i9.1712
Epinephrine also acts on beta cells and insulin secretion
Lina Zabuliene, Faculty of Medicine, Vilnius University, Vilnius LT-03101, Lithuania
Ioannis Ilias, Department of Endocrinology, “Hippokration” General Hospital, Athens GR-11527, Greece
ORCID number: Lina Zabuliene (0000-0002-7889-0862); Ioannis Ilias (0000-0001-5718-7441).
Author contributions: Zabuliene L and Ilias I researched for this work; Zabuliene L and Ilias I wrote the manuscript. Both authors agree to this publication.
Conflict-of-interest statement: Authors report that they have no conflict of interest to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ioannis Ilias, MD, PhD, Director, Department of Endocrinology, “Hippokration” General Hospital, No. 63 Evrou Street, Athens GR-11527, Greece. iiliasmd@yahoo.com
Received: October 18, 2023
Peer-review started: October 18, 2023
First decision: January 30, 2024
Revised: January 30, 2024
Accepted: March 4, 2024
Article in press: March 4, 2024
Published online: March 26, 2024
Processing time: 159 Days and 0.2 Hours

Abstract

In a recent review examining neurotransmitter modulation of insulin secretion, the significant impact of epinephrine was not addressed. Its primary action involves inhibiting insulin release via alpha-adrenergic receptors, thereby reducing the response to insulin secretion stimulators, through the activation of K+ channels and resulting in membrane hyperpolarization in beta cells.

Key Words: Epinephrine; Insulin; Islets; Glucose; Human

Core Tip: Among the neurotransmitters influencing insulin secretion, the role of epinephrine (EPI) might be underestimated. EPI mainly inhibits insulin release through alpha-adrenergic receptors, thereby attenuating the response to insulin secretion stimulators.
TO THE EDITOR

We have reviewed with interest the concise examination by Kong et al[1] of neurotransmitter influence on insulin secretion. While the authors extensively cover norepinephrine (NEPI), the role of epinephrine (EPI) is overlooked. Both EPI and NEPI, acting as neurotransmitters and hormones, are synthesized and released in the central and peripheral nervous systems and the adrenal medulla[2]. Despite NEPI's primary role as a neurotransmitter, the significance of EPI, which also functions as a hormone, should not be disregarded for its neurotransmitter functions. Hence, EPI's impact closely parallels that of NEPI, though with more pronounced peripheral effects[2].

EPI can prompt insulin release via beta-adrenergic receptor activation, involving adenylate cyclase, cAMP generation, and the cAMP Response Element-Binding Protein pathway[3]. However, its primary effect, mediated by alpha-adrenergic receptor activation, inhibits insulin secretion through the Protein kinase A pathway. This inhibition significantly moderates the response to insulin's strongest stimulants[4]. EPI achieves this by activating K+ channels, leading to hyperpolarization of pancreatic beta cell membranes[5,6].

The above concise overview of EPI's impact on insulin secretion complements the excellent and comprehensive review of neurotransmitter effects on insulin secretion[1].

Footnotes

Provenance and peer review: Unsolicited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Medicine, research and experimental

Country/Territory of origin: Greece

Peer-review report’s scientific quality classification

Grade A (Excellent): 0

Grade B (Very good): B

Grade C (Good): 0

Grade D (Fair): 0

Grade E (Poor): 0

P-Reviewer: Jovandaric MZ, Serbia S-Editor: Qu XL L-Editor: A P-Editor: Chen YX

References
1.  Kong CC, Cheng JD, Wang W. Neurotransmitters regulate β cells insulin secretion: A neglected factor. World J Clin Cases. 2023;11:6670-6679.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (2)]
2.  Kapalka GM.   Chapter 4-Substances Involved in Neurotransmission. Kapalka GM, editor. Nutritional and Herbal Therapies for Children and Adolescents. 2010; 71-99. Available from: https://www.sciencedirect.com/book/9780123749277/nutritional-and-herbal-therapies-for-children-and-adolescents.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Belgardt BF, Stoffel M. SIK2 regulates insulin secretion. Nat Cell Biol. 2014;16:210-212.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
4.  Hiatt N, Davidson MB, Chapman LW, Sheinkopf JA. Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors. Diabetes. 1978;27:550-553.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 7]  [Article Influence: 0.1]  [Reference Citation Analysis (0)]
5.  Zhang Y, Shumilina E, Häring HU, Lang F, Ullrich S. Epinephrine-induced hyperpolarization of pancreatic islet cells is sensitive to PI3K-PDK1 signaling. FEBS Lett. 2009;583:3101-3106.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 7]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
6.  Rorsman P, Ashcroft FM. Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men. Physiol Rev. 2018;98:117-214.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 420]  [Cited by in F6Publishing: 475]  [Article Influence: 67.9]  [Reference Citation Analysis (0)]