Leptin modulates electrophysiological characteristics and isoproterenol-induced arrhythmogenesis in atrial myocytes

Yung Kuo Lin, Yao Chang Chen, Jen Hung Huang, Yenn Jiang Lin, Shiang Suo Huang, Shih Ann Chen, Yi Jen Chen

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background: Obesity is an important risk factor for atrial fibrillation (AF). Leptin is an important adipokine. However, it is not clear whether leptin directly modulates the electrophysiological characteristics of atrial myocytes. Results: Whole cell patch clamp and indo-1 fluorescence were used to record the action potentials (APs) and ionic currents in isolated rabbit left atrial (LA) myocytes incubated with and without (control) leptin (100 nM) for 1 h to investigate the role of leptin on atrial electrophysiology. Leptin-treated LA myocytes (n = 19) had longer 20% of AP duration (28 ± 3 vs. 21 ± 2 ms, p <0.05), but similar 50% of AP duration (51 ± 4 vs. 50 ± 3 ms, p > 0.05), and 90% of AP duration (89 ± 5 vs. 94 ± 4 ms, p > 0.05), as compared to the control (n = 22). In the presence of isoproterenol (10 nM), leptin-treated LA myocytes (n = 21) showed a lower incidence (19% vs. 54.2%, p <0.05) of delayed afterdepolarization (DAD) than the control (n = 24). Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Leptin-treated and control LA myocytes exhibited a similar late sodium current, inward rectifier potassium current, transient outward current and L-type calcium current. In addition, the leptin-treated LA myocytes (n = 38) exhibited a smaller intracellular Ca§ssup§2+§esup§ transient (0.21 ± 0.01 vs. 0.26 ± 0.01 R410/485, p <0.05) and sarcoplasmic reticulum Ca§ssup§2+§esup§ content (0.35 ± 0.02 vs. 0.43 ± 0.03 R410/485, p <0.05) than the control LA myocytes (n = 42). Conclusions: Leptin regulates the LA electrophysiological characteristics and attenuates isoproterenol-induced arrhythmogenesis.

Original languageEnglish
Article number94
JournalJournal of Biomedical Science
Volume20
Issue number1
DOIs
Publication statusPublished - Dec 20 2013

Fingerprint

Leptin
Isoproterenol
Muscle Cells
Action Potentials
Sodium
Electrophysiology
Adipokines
Clamping devices
Sarcoplasmic Reticulum
Atrial Fibrillation
Potassium
Obesity
Fluorescence
Rabbits
Calcium
Incidence

Keywords

  • Adipokines
  • Atrial fibrillation
  • Epicardial fat
  • Leptin
  • Obesity

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Cell Biology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism
  • Pharmacology (medical)

Cite this

Leptin modulates electrophysiological characteristics and isoproterenol-induced arrhythmogenesis in atrial myocytes. / Lin, Yung Kuo; Chen, Yao Chang; Huang, Jen Hung; Lin, Yenn Jiang; Huang, Shiang Suo; Chen, Shih Ann; Chen, Yi Jen.

In: Journal of Biomedical Science, Vol. 20, No. 1, 94, 20.12.2013.

Research output: Contribution to journalArticle

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abstract = "Background: Obesity is an important risk factor for atrial fibrillation (AF). Leptin is an important adipokine. However, it is not clear whether leptin directly modulates the electrophysiological characteristics of atrial myocytes. Results: Whole cell patch clamp and indo-1 fluorescence were used to record the action potentials (APs) and ionic currents in isolated rabbit left atrial (LA) myocytes incubated with and without (control) leptin (100 nM) for 1 h to investigate the role of leptin on atrial electrophysiology. Leptin-treated LA myocytes (n = 19) had longer 20{\%} of AP duration (28 ± 3 vs. 21 ± 2 ms, p <0.05), but similar 50{\%} of AP duration (51 ± 4 vs. 50 ± 3 ms, p > 0.05), and 90{\%} of AP duration (89 ± 5 vs. 94 ± 4 ms, p > 0.05), as compared to the control (n = 22). In the presence of isoproterenol (10 nM), leptin-treated LA myocytes (n = 21) showed a lower incidence (19{\%} vs. 54.2{\%}, p <0.05) of delayed afterdepolarization (DAD) than the control (n = 24). Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Leptin-treated and control LA myocytes exhibited a similar late sodium current, inward rectifier potassium current, transient outward current and L-type calcium current. In addition, the leptin-treated LA myocytes (n = 38) exhibited a smaller intracellular Ca§ssup§2+§esup§ transient (0.21 ± 0.01 vs. 0.26 ± 0.01 R410/485, p <0.05) and sarcoplasmic reticulum Ca§ssup§2+§esup§ content (0.35 ± 0.02 vs. 0.43 ± 0.03 R410/485, p <0.05) than the control LA myocytes (n = 42). Conclusions: Leptin regulates the LA electrophysiological characteristics and attenuates isoproterenol-induced arrhythmogenesis.",
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T1 - Leptin modulates electrophysiological characteristics and isoproterenol-induced arrhythmogenesis in atrial myocytes

AU - Lin, Yung Kuo

AU - Chen, Yao Chang

AU - Huang, Jen Hung

AU - Lin, Yenn Jiang

AU - Huang, Shiang Suo

AU - Chen, Shih Ann

AU - Chen, Yi Jen

PY - 2013/12/20

Y1 - 2013/12/20

N2 - Background: Obesity is an important risk factor for atrial fibrillation (AF). Leptin is an important adipokine. However, it is not clear whether leptin directly modulates the electrophysiological characteristics of atrial myocytes. Results: Whole cell patch clamp and indo-1 fluorescence were used to record the action potentials (APs) and ionic currents in isolated rabbit left atrial (LA) myocytes incubated with and without (control) leptin (100 nM) for 1 h to investigate the role of leptin on atrial electrophysiology. Leptin-treated LA myocytes (n = 19) had longer 20% of AP duration (28 ± 3 vs. 21 ± 2 ms, p <0.05), but similar 50% of AP duration (51 ± 4 vs. 50 ± 3 ms, p > 0.05), and 90% of AP duration (89 ± 5 vs. 94 ± 4 ms, p > 0.05), as compared to the control (n = 22). In the presence of isoproterenol (10 nM), leptin-treated LA myocytes (n = 21) showed a lower incidence (19% vs. 54.2%, p <0.05) of delayed afterdepolarization (DAD) than the control (n = 24). Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Leptin-treated and control LA myocytes exhibited a similar late sodium current, inward rectifier potassium current, transient outward current and L-type calcium current. In addition, the leptin-treated LA myocytes (n = 38) exhibited a smaller intracellular Ca§ssup§2+§esup§ transient (0.21 ± 0.01 vs. 0.26 ± 0.01 R410/485, p <0.05) and sarcoplasmic reticulum Ca§ssup§2+§esup§ content (0.35 ± 0.02 vs. 0.43 ± 0.03 R410/485, p <0.05) than the control LA myocytes (n = 42). Conclusions: Leptin regulates the LA electrophysiological characteristics and attenuates isoproterenol-induced arrhythmogenesis.

AB - Background: Obesity is an important risk factor for atrial fibrillation (AF). Leptin is an important adipokine. However, it is not clear whether leptin directly modulates the electrophysiological characteristics of atrial myocytes. Results: Whole cell patch clamp and indo-1 fluorescence were used to record the action potentials (APs) and ionic currents in isolated rabbit left atrial (LA) myocytes incubated with and without (control) leptin (100 nM) for 1 h to investigate the role of leptin on atrial electrophysiology. Leptin-treated LA myocytes (n = 19) had longer 20% of AP duration (28 ± 3 vs. 21 ± 2 ms, p <0.05), but similar 50% of AP duration (51 ± 4 vs. 50 ± 3 ms, p > 0.05), and 90% of AP duration (89 ± 5 vs. 94 ± 4 ms, p > 0.05), as compared to the control (n = 22). In the presence of isoproterenol (10 nM), leptin-treated LA myocytes (n = 21) showed a lower incidence (19% vs. 54.2%, p <0.05) of delayed afterdepolarization (DAD) than the control (n = 24). Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Leptin-treated and control LA myocytes exhibited a similar late sodium current, inward rectifier potassium current, transient outward current and L-type calcium current. In addition, the leptin-treated LA myocytes (n = 38) exhibited a smaller intracellular Ca§ssup§2+§esup§ transient (0.21 ± 0.01 vs. 0.26 ± 0.01 R410/485, p <0.05) and sarcoplasmic reticulum Ca§ssup§2+§esup§ content (0.35 ± 0.02 vs. 0.43 ± 0.03 R410/485, p <0.05) than the control LA myocytes (n = 42). Conclusions: Leptin regulates the LA electrophysiological characteristics and attenuates isoproterenol-induced arrhythmogenesis.

KW - Adipokines

KW - Atrial fibrillation

KW - Epicardial fat

KW - Leptin

KW - Obesity

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