Analysis of liver metabolism in a rat model of heart failure

Abstract Background Cachexia, namely body wasting, is a common complication in cases of congestive heart failure (CHF). Although, neurohumoral and immune abnormalities are associated with the condition, precisely how the imbalance of catabolism and anabolism is responsible for the wasting process is...

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Bibliographic Details
Published in:International journal of cardiology 2012-11, Vol.161 (3), p.130-136
Main Authors: Kato, Takao, Niizuma, Shinichiro, Inuzuka, Yasutaka, Kawashima, Tsuneaki, Okuda, Junji, Kawamoto, Akira, Tamaki, Yodo, Iwanaga, Yoshitaka, Soga, Tomoyoshi, Kita, Toru, Kimura, Takeshi, Shioi, Tetsuo
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood Glucose - metabolism
Body Weight - physiology
Cachexia
Cardiology. Vascular system
Cardiovascular
Disease Models, Animal
Eating - physiology
Heart
Heart failure
Heart Failure - metabolism
Heart Failure - physiopathology
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Inflammation
Lipogenesis
Liver
Liver - metabolism
Male
Medical sciences
Rats
Rats, Inbred Dahl
Triglycerides - blood
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Summary:Abstract Background Cachexia, namely body wasting, is a common complication in cases of congestive heart failure (CHF). Although, neurohumoral and immune abnormalities are associated with the condition, precisely how the imbalance of catabolism and anabolism is responsible for the wasting process is not known. Methods We analyzed markers of cachexia in Dahl salt-sensitive rats which show marked hypertension with preserved systolic function at 11 weeks and CHF at 17–19 weeks of age. We also analyzed the change in hepatic metabolism associated with CHF since liver plays a central role in the systemic regulation of catabolism and anabolism. Results In CHF rats, a failure to grow was observed and blood hepatic protein levels were decreased associated with increased blood proinflammatory cytokine levels, indicating that Dahl rats serve as a model of cardiac cachexia. Food intake was reduced, and blood sugar and insulin levels were decreased. Despite the apparent fasting condition, blood fatty acid levels were decreased and triglycerides levels were increased. In CHF rats, liver incorporated more glucose, the gene expression related to gluconeogenesis was decreased, the gene expression related to lipogenesis was increased, and the triglyceride content of the liver was increased. The paradoxical production of triglycerides synthesis in fasting rats was associated with a proinflammatory response in liver. Conclusions The Dahl salt-sensitive rat can be used as a model of cardiac cachexia. The cachexia was associated with abnormal hepatic metabolism that might work as a maladaptive response during the progression of CHF.
ISSN:0167-5273
1874-1754
DOI:10.1016/j.ijcard.2011.07.056