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Diabetes impairs heart mitochondrial function without changes in resting cardiac performance.

Silvina S Bombicino1, Darío E Iglesias1, Ivana A Rukavina Mikusic1

  • 1University of Buenos Aires, Institute of Biochemistry and Molecular Medicine (IBIMOL; UBA-CONICET), School of Pharmacy and Biochemistry, Physical Chemistry Division, Buenos Aires, Argentina.

The International Journal of Biochemistry & Cell Biology
|September 30, 2016
PubMed
Summary

Diabetic cardiomyopathy involves impaired heart mitochondrial function and reduced oxygen consumption, preceding cardiac performance changes. This suggests mitochondrial dysfunction is an early indicator of diabetic heart failure.

Keywords:
Cardiac and mitochondrial dysfunctionIsoproterenol (ISO)Mitochondrial nitric oxide synthase (mtNOS)Oxidative stressStreptozotocin (STZ)Type I diabetes

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Diabetology

Background:

  • Diabetes mellitus is linked to cardiac contractile dysfunction, potentially stemming from mitochondrial deterioration.
  • Diabetic cardiomyopathy is a distinct condition not caused by hypertension or coronary artery disease.
  • Mitochondrial dysfunction is hypothesized to precede the development of diabetic cardiomyopathy.

Purpose of the Study:

  • To investigate cardiac performance and mitochondrial function in an experimental model of type 1 diabetes.
  • To determine if mitochondrial impairment precedes cardiac dysfunction in diabetes.

Main Methods:

  • Type 1 diabetes was induced in rats using Streptozotocin (STZ).
  • Cardiac performance and mitochondrial respiration (oxygen consumption, ADP/O ratio, respiratory complex activities) were assessed.
  • Mitochondrial hydrogen peroxide (H2O2) and nitric oxide (NO) production, tyrosine nitration, and manganese superoxide dismutase (Mn-SOD) activity were measured.

Main Results:

  • Diabetic rats exhibited reduced heart oxygen consumption and impaired mitochondrial respiration.
  • Mitochondrial dysfunction included decreased state 3 respiration, lower ADP/O ratio, and reduced respiratory complex activities.
  • Increased mitochondrial H2O2 and NO production, elevated tyrosine nitration, and decreased Mn-SOD activity were observed in diabetic hearts.
  • Contractile, inotropic, and lusitropic reserves were diminished in diabetic rats upon beta-adrenergic stimulation.
  • These changes occurred without heart hypertrophy or alterations in resting cardiac function.

Conclusions:

  • Sustained hyperglycemia leads to decreased mitochondrial oxygen consumption and oxidative phosphorylation efficiency in the heart.
  • Increased mitochondrial H2O2 and NO production contribute to cardiac compromise under workload.
  • Mitochondrial dysfunction, characterized by altered ROS/RNS signaling, may precede diabetic cardiac failure.