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Pathological hypertrophy and cardiac dysfunction are linked to aberrant endogenous unsaturated fatty acid metabolism

Loreta Casquel De Tomasi1,2, Dijon Henrique Salomé Campos1, Paula Grippa Sant'Ana1

  • 1Department of Internal Medicine, São Paulo State University, Botucatu, São Paulo, Brazil.

Plos One
|March 2, 2018
PubMed

Insights

A high-unsaturated fatty acid (HUFA) diet did not reverse cardiac dysfunction or hypertrophy in rats. Aberrant unsaturated fatty acid metabolism, not just reduced oxidation, characterizes hypertrophied hearts.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Physiology
  • Cardiac Pathophysiology

Background:

  • Pathological cardiac hypertrophy impairs lipid metabolism, potentially causing cardiac dysfunction.
  • Previous studies on high saturated fat diets yielded inconclusive results regarding lipid metabolism in cardiac hypertrophy.

Purpose of the Study:

  • To investigate if a high-unsaturated fatty acid (HUFA) diet can restore impaired lipid metabolism and normalize diastolic dysfunction in pathologically hypertrophied hearts.
  • To determine the effects of HUFA diet on cardiac lipid pools and metabolic gene expression in a rat model of cardiac hypertrophy.

Main Methods:

  • Male Wistar rats underwent supra-valvar aortic stenosis (SVAS) or sham surgery.
  • Following confirmation of hypertrophy and diastolic dysfunction, rats received either a normolipidic or HUFA diet.
  • Cardiac function, hypertrophy, lipid metabolism (enzymatic activity, gene expression, mass spectrometry), and tissue fatty acid composition were assessed.

Main Results:

  • The HUFA diet failed to normalize diastolic dysfunction (E/A ratios) or reduce cardiac hypertrophy in SVAS rats.
  • Both normolipidic and HUFA-fed SVAS hearts showed increased glycolytic enzyme activity and decreased fatty acid oxidation gene expression.
  • Mass spectrometry revealed depletion of endogenous unsaturated fatty acids (linoleate, oleate) in SVAS hearts, which the HUFA diet did not restore in cardiac tissue.

Conclusions:

  • Aberrant unsaturated fatty acid metabolism, alongside reduced fatty acid oxidation, is a key feature of pathologically hypertrophied hearts.
  • A HUFA diet is insufficient to reverse metabolic remodeling, diastolic dysfunction, or cardiac hypertrophy in this model.
  • Unsaturated fatty acids may be preferentially partitioned to adipose tissue, limiting their availability for cardiac restoration.

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