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GLP-1 receptor agonist liraglutide protects cardiomyocytes from IL-1β-induced metabolic disturbance and mitochondrial

Lili Zhang1, Jiali Tian2, Sujuan Diao3

  • 1Department of Cardiology, The People's Hospital of Longhua, The Affiliated Hospital of Southern Medical University, Shenzhen City, Guangdong Province, 518109, China; Department of Cardiology, Heilongjiang Academy of Medical Science, Harbin City, Heilongjiang Province, 150086, China.

Chemico-Biological Interactions
|September 8, 2020
PubMed

Insights

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) like Liraglutide protect heart cells from inflammation. Liraglutide preserves mitochondrial function and cardiac metabolism by activating AMPK, suggesting therapeutic potential for heart failure.

Area of Science:

  • Cardiology
  • Endocrinology
  • Molecular Biology

Background:

  • Cardiac inflammation is a key factor in heart failure development, often involving oxidative stress that impairs cardiac metabolism and mitochondrial function.
  • Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), used for type 2 diabetes, show promise in managing cardiovascular complications.
  • Liraglutide, a long-acting GLP-1 RA, exhibits potential cardioprotective effects.

Purpose of the Study:

  • To investigate the protective mechanisms of Liraglutide in cultured cardiomyocytes against inflammation-induced damage.
  • To elucidate the role of GLP-1 receptor signaling and AMPK activation in Liraglutide's cardioprotective effects.

Main Methods:

  • HL-1 cardiomyocytes were treated with IL-1β and Liraglutide.
  • Assessed reactive oxygen species (ROS) production, NADPH oxidase 4 (NOX-4) expression, mitochondrial membrane potential, and ATP production.
  • Utilized Seahorse analysis for cellular respiration and measured triglyceride accumulation and adiponectin secretion.
  • Investigated the phosphorylation of AMPK, ACC, and the expression of PGC-1α, CPT-1, and DGAT1.
  • Examined the effect of AMPK inhibition using Compound C.

Main Results:

  • Liraglutide reduced IL-1β-induced ROS production and NOX-4 expression in cardiomyocytes expressing GLP-1 receptors.
  • Liraglutide preserved mitochondrial function by maintaining membrane potential, ATP production, and respiration rates.
  • Liraglutide mitigated aberrant triglyceride accumulation and adiponectin secretion.
  • Liraglutide's protective effects were linked to AMPK activation, as inhibiting AMPK abolished Liraglutide's benefits on ATP production and triglyceride levels.

Conclusions:

  • Liraglutide demonstrates significant cardioprotective effects in cultured cardiomyocytes by ameliorating inflammation-induced oxidative stress and metabolic dysfunction.
  • The mechanism involves the activation of the AMPK pathway, highlighting its crucial role in Liraglutide's therapeutic action.
  • Liraglutide holds therapeutic promise for modulating cardiac inflammation and potentially treating heart failure.
Keywords:
AMPKCardiomyocytesGLP-1 receptorLiraglutideMitochondrial function

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