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Cardiac transcriptome analysis in obesity-related hypertension
Pierre Philip-Couderc1, Fatima Smih, Michel Pelat
1INSERM U586, Faculté de Médecine, Laboratoire de Pharmacologie Médicale et Clinique, 37 Allées Jules Guesde. 31073 Toulouse Cedex. France.
Hypertension (Dallas, Tex. : 1979)
|March 8, 2003
Summary
Obesity-induced hypertension rapidly alters heart gene expression, even without significant structural changes. This early molecular response in the right atrium and left ventricle may precede long-term heart problems.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genomics
Background:
- Obesity is linked to hypertension, increased heart rate, and reduced heart rate variability.
- The impact of obesity-related hypertension on cardiac gene regulation is not well understood.
Purpose of the Study:
- To investigate the effects of short-term, diet-induced obesity and hypertension on gene expression in the canine heart.
- To identify specific genes and pathways affected by obesity-related cardiac changes.
Main Methods:
- A high-fat diet was used to induce obesity and hypertension in dogs over 9 weeks.
- Subtractive hybridization and custom microarrays were employed to compare gene expression in the atria and ventricles of obese hypertensive and control dogs.
- Differential gene expression was validated using Northern blot and real-time quantitative polymerase chain reaction.
Main Results:
- The high-fat diet caused significant weight gain, increased blood pressure, and elevated heart rate, but not significant changes in left ventricular mass.
- Thirty-eight differentially expressed genes were identified in the hearts of obese hypertensive dogs.
- Affected genes were involved in metabolism, cell signaling, ionic regulation, cell proliferation, protein synthesis, and tissue remodeling, with 11 cDNAs encoding proteins of unknown function.
Conclusions:
- Short-term obesity-related hypertension induces significant alterations in cardiac gene expression in both the right atrium and left ventricle.
- These early gene expression changes may contribute to functional heart alterations and potentially lead to long-term structural changes like left ventricular hypertrophy.