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Imagine adding a small amount of sugar to a glass of water, stirring until all the sugar has dissolved, and then adding a bit more. You can repeat this process until the sugar concentration of the solution reaches its natural limit, a limit determined primarily by the relative strengths of the solute-solute, solute-solvent, and solvent-solvent attractive forces. You can be certain that you have reached this limit because, no matter how long you stir the solution, undissolved sugar remains. The...
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Sirt1 counteracts decrease in membrane phospholipid unsaturation and diastolic dysfunction during saturated fatty

Tsunehisa Yamamoto1, Jin Endo2, Masaharu Kataoka1

  • 1Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Journal of Molecular and Cellular Cardiology
|May 31, 2019
PubMed
Summary

Cardiac Sirt1 (Silent information regulator 1) protects against saturated fatty acid (SFA) overload by regulating Scd1 (stearoyl-CoA desaturase-1) gene expression, improving heart function.

Keywords:
Diastolic dysfunctionMembrane fatty acid compositionSaturated fatty acidSirt1Stearoyl-CoA desaturase-1

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Regulation
  • Molecular Cardiology

Background:

  • Dietary fat composition influences membrane phospholipid fatty acid (FA) profiles.
  • Saturated fatty acids (SFA) inhibit Sirt1 activity, while monounsaturated fatty acids (MUFA) counteract this effect.

Purpose of the Study:

  • To investigate the role of Sirt1 in maintaining membrane phospholipid FA homeostasis during SFA overload.
  • To understand the molecular mechanisms linking Sirt1, FA composition, and cardiac function.

Main Methods:

  • Utilized Sirt1-deficient mice and cultured cardiomyocytes subjected to SFA overload (palmitate).
  • Assessed membrane FA composition (SFA/MUFA ratio), gene expression (Sirt1, LXR, Scd1), and left ventricular (LV) diastolic function.
  • Investigated the effects of Sirt1 knockdown (KD), Scd1 overexpression, LXR knockdown, and pharmacological agents (NMN, T0901317).

Main Results:

  • Sirt1 deficiency worsened membrane SFA/MUFA ratio and LV diastolic function in mice on a high-fat diet.
  • Sirt1 KD in cardiomyocytes increased SFA/MUFA ratio, linked to reduced LXR-target gene expression, including Scd1.
  • Overexpression of Scd1 or treatment with NMN (which activates Sirt1) lowered the SFA/MUFA ratio.
  • LXR activation was crucial for Sirt1's effect on Scd1 expression and FA composition.

Conclusions:

  • Cardiac Sirt1 mitigates SFA overload-induced diastolic dysfunction by regulating the LXR-Scd1 pathway.
  • Sirt1 maintains membrane phospholipid unsaturation through transcriptional control of Scd1.
  • Targeting Sirt1 or LXR pathways may offer therapeutic strategies for SFA-induced cardiac issues.