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

1 Scopus citations

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)
Article number2660
JournalInternational journal of molecular sciences
Volume20
Issue number11
DOIs
StatePublished - Jun 1 2019

Keywords

  • ATP-sensitive potassium (K) 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

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