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Published on: December 2, 2016
Cardiac hypertrophy-related pathways in obesity
Wei-Kung Chen1, Yu-Lan Yeh, Yueh-Min Lin
1Graduate Institute of Clinical Medical Science, China Medical University, Taichung 40440, Taiwan, Republic of China.
Obesity activates cardiac hypertrophy pathways, increasing heart weight and specific protein markers like ANP, BNP, and TNFα in obese rats. These findings reveal mechanisms behind obesity-induced cardiac changes.
Area of Science:
- Cardiology
- Metabolic Disorders
- Molecular Biology
Background:
- Obesity is linked to cardiac hypertrophy, but the underlying molecular pathways are not fully understood.
- Identifying these pathways is crucial for understanding and treating obesity-related heart disease.
Purpose of the Study:
- To investigate cardiac hypertrophy markers and pathways in obese rats.
- Specifically evaluate atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), tumor necrosis factor-alpha (TNFα), and signaling pathways including IL-6-STAT3, IL-6-MEK5-ERK5, and calcineurin-NFAT3.
Main Methods:
- Used obese and lean Zucker rats for comparison.
- Assessed cardiac characteristics via heart weight index, echocardiography, and histology.
- Quantified protein and gene expression of hypertrophy markers and pathways using RT-PCR and Western blotting.
Main Results:
- Obese rats exhibited increased heart weight, left ventricle weight, wall thickness, and systolic blood pressure compared to lean controls.
- Elevated levels of ANP, BNP, TNFα, IL-6, STAT3, p-STAT3, MEK5, ERK-5, p-ERK-5, calcineurin, and NFAT3 were observed in obese rat hearts.
- Hypertrophy-related markers and pathways were significantly more active in obese rats.
Conclusions:
- Obesity activates specific cardiac hypertrophy markers (ANP, BNP, TNFα) and signaling pathways (IL-6-STAT3, IL-6-MEK5-ERK5, calcineurin-NFAT3).
- These activated pathways offer potential molecular mechanisms for cardiac hypertrophy and pathological changes associated with obesity.
- This study provides insights into the molecular basis of obesity-induced heart disease.
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