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Related Experiment Videos

Impaired SERCA function contributes to cardiomyocyte dysfunction in insulin resistant rats.

Loren E Wold1, Kaushik Dutta, Meredith M Mason

  • 1Department of Pharmacology, Physiology and Therapeutics, University of North Dakota, Grand Forks, ND, USA.

Journal of Molecular and Cellular Cardiology
|May 10, 2005
PubMed
Summary

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Impaired sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity slows cardiomyocyte relaxation in insulin-resistant rats before type 2 diabetes develops. This early cellular dysfunction may precede heart failure in metabolic disorders.

Area of Science:

  • Cardiology
  • Metabolic Disorders
  • Cellular Physiology

Background:

  • Ventricular dysfunction is an early complication in type 2 diabetes, but its underlying cellular mechanisms remain unclear.
  • Previous studies identified cardiomyocyte dysfunction in diet-induced insulin-resistant rats preceding overt type 2 diabetes.
  • This study investigates cellular mechanisms of slowed cardiomyocyte relaxation in insulin-resistant rats.

Purpose of the Study:

  • To determine the cellular mechanisms responsible for slowed cardiomyocyte relaxation in sucrose (SU)-fed rats, an animal model of insulin resistance.
  • To investigate the roles of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and Na+/Ca2+ exchange (NCX) in cardiomyocyte dysfunction.

Main Methods:

  • Adult male Wistar rats were fed sucrose (SU) or starch (ST) diets for 9-12 weeks to induce insulin resistance.

Related Experiment Videos

  • Isolated ventricular myocytes were assessed for shortening and relengthening properties using fluo-3/AM for Ca2+ measurements.
  • SERCA and NCX function were evaluated by measuring Ca2+ uptake and release, and protein levels of key proteins (SERCA, NCX, phospholamban) were analyzed.

    • Main Results:

    • SU-fed rats exhibited significantly slower myocyte shortening and relengthening compared to ST-fed controls.
    • Ca2+ uptake by SERCA was significantly impaired in SU myocytes, while caffeine-releasable Ca2+ and NCX function were normal.
    • Protein levels of SERCA, NCX, and phospholamban were unaffected by SU-feeding, indicating functional impairment rather than altered expression.

    Conclusions:

    • Impaired SERCA activity, independent of protein content, contributes to cardiomyocyte dysfunction in insulin-resistant animals.
    • Normal NCX function and expression suggest a specific defect in SERCA-mediated Ca2+ reuptake.
    • These findings highlight early Ca2+ regulatory changes in cardiomyocytes as a potential common pathway in insulin resistance-related disorders.