title: Effect of infliximab on metabolic disorders induced by Walker-256 tumor in rats.
abstract: BACKGROUND
  The purpose of this study was to investigate the effect of infliximab, an anti-tumor necrosis factor α (TNFα) monoclonal antibody, on the progression of cachexia and several metabolic parameters affected by the Walker-256 tumor in rats.
  
  
  METHODS
  Infliximab (0.5 mg/kg) was ip administered, twice a day, beginning at the day in which the Walker-256 tumor cells were inoculated. After 12 days of treatment, the tumor growth, some parameters of cachexia/anorexia, the blood levels of triacylglycerol, glucose, lactate and urea, the peripheral response to insulin and the hepatic glycolysis and gluconeogenesis were investigated. The peripheral response to insulin was evaluated by the insulin tolerance test and the glycolysis and gluconeogenesis in isolated perfused liver.
  
  
  RESULTS
  The treatment with infliximab did not alter the growth of the Walker-256 tumor, but attenuated (p < 0.05) the reduction of body weight and prevented (p < 0.05) the loss of retroperitoneal adipose tissue induced by the tumor. Moreover, treatment with infliximab tended to minimize the loss of gastrocnemius muscle, the reduction in food intake, the peripheral response to insulin and the liver gluconeogenesis from alanine, as well as the increased blood triacylglycerol, caused by the tumor. In contrast, treatment with infliximab did not attenuate the reduction in hepatic glycolysis and glycemia, nor did it minimize the rise in blood levels of lactate and urea induced by the tumor.
  
  
  CONCLUSIONS
  The treatment with infliximab ameliorated some changes associated with cachexia, such as the reduction of adipose tissue and body weight, suggesting that TNFα plays a significant role in mediating these changes induced by the tumor. In addition, infliximab tended to improve or had no effect on other metabolic parameters affected by the Walker-256 tumor, suggesting that other mediators or tumor-related events are involved in these disorders.
authors.affiliation: Department of Physiological Sciences, State University of Londrina, 86051-990, Londrina, PR, Brazil. hmedri@uel.br.
authors.forename: Daniele R
authors.initials: DR
authors.lastname: Miksza
authors.forename: Camila O
authors.initials: CO
authors.lastname: de Souza
authors.forename: Hely
authors.initials: H
authors.lastname: de Morais
authors.forename: Aline F
authors.initials: AF
authors.lastname: da Rocha
authors.forename: Gláucia R
authors.initials: GR
authors.lastname: Borba-Murad
authors.forename: Roberto B
authors.initials: RB
authors.lastname: Bazotte
authors.forename: Helenir M
authors.initials: HM
authors.lastname: de Souza
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D001786:Blood Glucose / Q000187:drug effects; D002100:Cachexia / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D002279:Carcinoma 256, Walker / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D004435:Eating / Q000187:drug effects; D005943:Gluconeogenesis / Q000187:drug effects; D006019:Glycolysis / Q000187:drug effects; D000069285:Infliximab; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051381:Rats; D014280:Triglycerides / Q000097:blood; D014508:Urea / Q000097:blood
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D001786:Blood Glucose; D014280:Triglycerides; D019344:Lactic Acid; D014508:Urea; D000069285:Infliximab