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Fibroblast growth factor 21 (FGF21) therapy attenuates left ventricular dysfunction and metabolic disturbance by

P Tanajak1,2,3, P Sa-Nguanmoo1,2,3, X Wang4

  • 1Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

Acta Physiologica (Oxford, England)
|April 28, 2016
PubMed
Abstract

Insights

Long-term fibroblast growth factor 21 (FGF21) therapy improved heart function in obese rats by reducing insulin resistance and enhancing metabolic regulation. This study highlights FGF21

Area of Science:

  • Metabolic regulation and cardiovascular health.
  • Endocrinology and obesity research.
  • Mitochondrial function and redox homeostasis.

Background:

  • Fibroblast growth factor 21 (FGF21) is a key metabolic regulator with known cardioprotective effects.
  • Obesity and insulin resistance often lead to cardiac dysfunction and FGF21 resistance.
  • The impact of sustained FGF21 administration on cardiac health in FGF21-resistant obese models remains under-explored.

Purpose of the Study:

  • To investigate the effects of long-term fibroblast growth factor 21 (FGF21) administration on cardiac function in obese, insulin-resistant rats.
  • To determine if FGF21 therapy can overcome FGF21 resistance and improve metabolic parameters.
  • To elucidate the underlying mechanisms of FGF21-mediated cardioprotection in this model.

Main Methods:

  • Obese, insulin-resistant rats were established using a high-fat diet (HFD) for 12 weeks.
  • Rats received either vehicle (HFV) or recombinant human FGF21 (rhFGF21; HFF) via intraperitoneal injection for 28 days.
  • Comprehensive analysis included metabolic parameters, inflammation markers, oxidative stress (MDA), heart rate variability (HRV), left ventricular (LV) function, cardiac mitochondrial function (FAO, redox), and apoptosis signaling.

Main Results:

  • High-fat diet-fed rats exhibited dyslipidemia, insulin resistance, elevated plasma FGF21, inflammation (TNF-α), oxidative stress (MDA), depressed HRV, and impaired cardiac and mitochondrial function.
  • FGF21 treatment (HFF) significantly improved metabolic profiles, reduced inflammation and oxidative stress, and enhanced HRV and cardiac/mitochondrial function.
  • FGF21 therapy upregulated anti-apoptotic (Bcl-2) and FAO-related proteins (PGC-1α, CPT-1) in the heart.

Conclusions:

  • Long-term FGF21 therapy effectively attenuates both FGF21 and insulin resistance in obese rats.
  • FGF21 exerts significant cardioprotective effects by improving cardiometabolic regulation.
  • The cardioprotective mechanisms involve the activation of anti-apoptotic and cardiac mitochondrial fatty acid oxidation (FAO) signaling pathways.
Keywords:
FGF21 resistancecardiac functionfatty acid β-oxidationfibroblast growth factor 21 (FGF21)mitochondriaobesity-insulin resistance

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