Reduced-energy diet improves survival of obese KKAy mice with viral myocarditis: Induction of cardiac adiponectin expression
Abstract
Obesity is an important risk factor for heart disease. Whether weight loss affects the severity of heart failure induced by viral myocarditis is a matter of debate. We hypothesized that weight loss could improve cardiac dysfunction by inducing cardiac expression of a cardioprotective cytokine, adiponectin. We examined the relationship between weight loss by food restriction and heart failure due to viral myocarditis in obese KKAy mice. We intraperitoneally injected encephalomyocarditis virus (500 plaque-forming units/mouse) into KKAy mice fed ad libitum as a control (CF) or 60% restriction of that eaten by ad libitum (RF). The 14-day survival rate was 0% in FF, whereas it was 23% in RF (P<0.01). Heart weight/body weight ratio in RF was lower than that in FF on day 5 after viral inoculation (P<0.05). Histological scores for myocardial necrosis and inflammation on day 5 were significantly lower in RF than in FF (P<0.05). Circulating adiponectin level on day 0 was significantly elevated in RF compared with that in FF (32+9 vs. 22+2 microg/mL, P<0.05). Comparative expression of cardiac adiponectin mRNA in RF was significantly higher than that in FF (5.1+0.3 vs. 1+0.2, P<0.05). Cardiac tumor necrosis factor-alpha (TNF-alpha) mRNA in RF was significantly decreased compared with that in FF on day 5 (P<0.05). Cardiac expression of nuclear factor kappa B was reduced and that of peroxisome proliferator-activated receptor gamma mRNA was increased in RF in comparison with FF on day 0. Cardiac adiponectin mRNA was negatively correlated with cardiac TNF-alpha mRNA (r=-0.555; P=0.0097). Weight loss improved the survival and myocardial damage in obese mice with viral myocarditis, with cardiac induction of adiponectin. The induction of adiponectin might provide benefit through a cardioprotective effect against acute heart failure due to viral myocarditis in obese subjects.
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Myocardial necrosis in obese mice with viral myocarditis was attenuated upon endogenous cardiac induction of adiponectin expression, suggesting this may represent a compensatory protective response.
“Furthermore, myocardial necrosis in obese mice with viral myocarditis was attenuated upon endogenous cardiac induction of adiponectin expression, suggesting this may represent a compensatory protective response (167, 338, 340).”
From Cardiac remodeling in obesity (2008) · cites this paper as [167]
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- Authors
- Kanda, T., Saegusa, S., Takahashi, T., Sumino, H., Morimoto, S., Nakahashi, T., Iwai, K., & Matsumoto, M.
- Affiliations
- Kanazawa Medical University (JP)
- Gunma University (JP)
- Venue
- International Journal of Cardiology
- Publisher
- Elsevier BV
- Published
- 2007-07
- Volume
- 119
- Issue
- 3
- Pages
- 310-318
- ISSN
- 0167-5273 (ISSN-L)
- OpenAlex
- W1982596194
- Cited by
- 19
- References
- 38
- Citations by year
- 2024: 2 · 2015: 2 · 2014: 5 · 2013: 1
- FWCI
- 1.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Kanazawa University
- Kanazawa Medical University
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- viral myocarditis, obesity, weight loss, dietary restriction, adiponectin, KK-Ay mice, encephalomyocarditis virus, heart failure, TNF-α, NF-κB, PPARγ, myocarditis, myocardial necrosis, cardioprotection
- MeSH terms
- Animals, Disease Models, Animal, Encephalomyocarditis virus, Female, Mice, Obese, Myocarditis, Obesity, RNA, Messenger, Weight Loss, Survival Analysis, Cardiovirus Infections, Caloric Restriction, Mice, Adiponectin
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