Leptin-induced Trafficking of KATP Channels

A Mechanism to Regulate Pancreatic β-cell Excitability and Insulin Secretion

Veronica Cochrane, Show-Ling Shyng

Research output: Contribution to journalReview article

Abstract

The adipocyte hormone leptin was first recognized for its actions in the central nervous system to regulate energy homeostasis but has since been shown to have direct actions on peripheral tissues. In pancreatic β-cells leptin suppresses insulin secretion by increasing KATP channel conductance, which causes membrane hyperpolarization and renders β-cells electrically silent. However, the mechanism by which leptin increases KATP channel conductance had remained unresolved for many years following the initial observation. Recent studies have revealed that leptin increases surface abundance of KATP channels by promoting channel trafficking to the β-cell membrane. Thus, KATP channel trafficking regulation has emerged as a mechanism by which leptin increases KATP channel conductance to regulate β-cell electrical activity and insulin secretion. This review will discuss the leptin signaling pathway that underlies KATP channel trafficking regulation in β-cells.

Original languageEnglish (US)
JournalInternational journal of molecular sciences
Volume20
Issue number11
DOIs
StatePublished - May 30 2019

Fingerprint

KATP Channels
insulin
secretions
Insulin
Leptin
Hormones
Neurology
Cell membranes
cells
Tissue
Membranes
homeostasis
central nervous system
hormones
Adipocytes
Homeostasis
Central Nervous System
Cell Membrane
Observation
membranes

Keywords

  • ATP-sensitive potassium (KATP) channel
  • Insulin secretion
  • Leptin
  • β-cell

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

@article{8aed6468f40f4e798867a0509719860c,
title = "Leptin-induced Trafficking of KATP Channels: A Mechanism to Regulate Pancreatic β-cell Excitability and Insulin Secretion",
abstract = "The adipocyte hormone leptin was first recognized for its actions in the central nervous system to regulate energy homeostasis but has since been shown to have direct actions on peripheral tissues. In pancreatic β-cells leptin suppresses insulin secretion by increasing KATP channel conductance, which causes membrane hyperpolarization and renders β-cells electrically silent. However, the mechanism by which leptin increases KATP channel conductance had remained unresolved for many years following the initial observation. Recent studies have revealed that leptin increases surface abundance of KATP channels by promoting channel trafficking to the β-cell membrane. Thus, KATP channel trafficking regulation has emerged as a mechanism by which leptin increases KATP channel conductance to regulate β-cell electrical activity and insulin secretion. This review will discuss the leptin signaling pathway that underlies KATP channel trafficking regulation in β-cells.",
keywords = "ATP-sensitive potassium (KATP) channel, Insulin secretion, Leptin, β-cell",
author = "Veronica Cochrane and Show-Ling Shyng",
year = "2019",
month = "5",
day = "30",
doi = "10.3390/ijms20112660",
language = "English (US)",
volume = "20",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "11",

}

TY - JOUR

T1 - Leptin-induced Trafficking of KATP Channels

T2 - A Mechanism to Regulate Pancreatic β-cell Excitability and Insulin Secretion

AU - Cochrane, Veronica

AU - Shyng, Show-Ling

PY - 2019/5/30

Y1 - 2019/5/30

N2 - The adipocyte hormone leptin was first recognized for its actions in the central nervous system to regulate energy homeostasis but has since been shown to have direct actions on peripheral tissues. In pancreatic β-cells leptin suppresses insulin secretion by increasing KATP channel conductance, which causes membrane hyperpolarization and renders β-cells electrically silent. However, the mechanism by which leptin increases KATP channel conductance had remained unresolved for many years following the initial observation. Recent studies have revealed that leptin increases surface abundance of KATP channels by promoting channel trafficking to the β-cell membrane. Thus, KATP channel trafficking regulation has emerged as a mechanism by which leptin increases KATP channel conductance to regulate β-cell electrical activity and insulin secretion. This review will discuss the leptin signaling pathway that underlies KATP channel trafficking regulation in β-cells.

AB - The adipocyte hormone leptin was first recognized for its actions in the central nervous system to regulate energy homeostasis but has since been shown to have direct actions on peripheral tissues. In pancreatic β-cells leptin suppresses insulin secretion by increasing KATP channel conductance, which causes membrane hyperpolarization and renders β-cells electrically silent. However, the mechanism by which leptin increases KATP channel conductance had remained unresolved for many years following the initial observation. Recent studies have revealed that leptin increases surface abundance of KATP channels by promoting channel trafficking to the β-cell membrane. Thus, KATP channel trafficking regulation has emerged as a mechanism by which leptin increases KATP channel conductance to regulate β-cell electrical activity and insulin secretion. This review will discuss the leptin signaling pathway that underlies KATP channel trafficking regulation in β-cells.

KW - ATP-sensitive potassium (KATP) channel

KW - Insulin secretion

KW - Leptin

KW - β-cell

UR - http://www.scopus.com/inward/record.url?scp=85066939476&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85066939476&partnerID=8YFLogxK

U2 - 10.3390/ijms20112660

DO - 10.3390/ijms20112660

M3 - Review article

VL - 20

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 11

ER -