title: 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 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.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: Takao
authors.initials: T
authors.lastname: Kato
authors.forename: Shinichiro
authors.initials: S
authors.lastname: Niizuma
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Inuzuka
authors.forename: Tsuneaki
authors.initials: T
authors.lastname: Kawashima
authors.forename: Junji
authors.initials: J
authors.lastname: Okuda
authors.forename: Akira
authors.initials: A
authors.lastname: Kawamoto
authors.forename: Yodo
authors.initials: Y
authors.lastname: Tamaki
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Iwanaga
authors.forename: Tomoyoshi
authors.initials: T
authors.lastname: Soga
authors.forename: Toru
authors.initials: T
authors.lastname: Kita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kimura
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Shioi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D004195:Disease Models, Animal; D004435:Eating / Q000502:physiology; D006333:Heart Failure / Q000378:metabolism* / Q000503:physiopathology; D008099:Liver / Q000378:metabolism*; D008297:Male; D051381:Rats; D020303:Rats, Inbred Dahl; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D014280:Triglycerides