PMID- 24145090
OWN - NLM
STAT- MEDLINE
DCOM- 20140613
LR  - 20200106
IS  - 2299-5684 (Electronic)
IS  - 1734-1140 (Linking)
VI  - 65
IP  - 4
DP  - 2013
TI  - Effect of infliximab on metabolic disorders induced by Walker-256 tumor in rats.
PG  - 960-9
AB  - BACKGROUND: The purpose of this study was to investigate the effect of 
      infliximab, an anti-tumor necrosis factor alpha (TNFalpha) 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. CONCLUSION: The treatment with infliximab ameliorated some changes 
      associated with cachexia, such as the reduction of adipose tissue and body 
      weight, suggesting that TNFalpha 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.
FAU - Miksza, Daniele R
AU  - Miksza DR
AD  - Department of Physiological Sciences, State University of Londrina, 86051-990, 
      Londrina, PR, Brazil. hmedri@uel.br.
FAU - de Souza, Camila O
AU  - de Souza CO
FAU - de Morais, Hely
AU  - de Morais H
FAU - da Rocha, Aline F
AU  - da Rocha AF
FAU - Borba-Murad, Glaucia R
AU  - Borba-Murad GR
FAU - Bazotte, Roberto B
AU  - Bazotte RB
FAU - de Souza, Helenir M
AU  - de Souza HM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Pharmacol Rep
JT  - Pharmacological reports : PR
JID - 101234999
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Blood Glucose)
RN  - 0 (Triglycerides)
RN  - 33X04XA5AT (Lactic Acid)
RN  - 8W8T17847W (Urea)
RN  - B72HH48FLU (Infliximab)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology/therapeutic use
MH  - Antibodies, Monoclonal/*pharmacology/therapeutic use
MH  - Blood Glucose/drug effects
MH  - Cachexia/blood/complications/*drug therapy
MH  - Carcinoma 256, Walker/blood/complications/*drug therapy
MH  - Eating/drug effects
MH  - Gluconeogenesis/drug effects
MH  - Glycolysis/drug effects
MH  - Infliximab
MH  - Lactic Acid/blood
MH  - Liver/drug effects/metabolism
MH  - Male
MH  - Rats
MH  - Triglycerides/blood
MH  - Urea/blood
EDAT- 2013/10/23 06:00
MHDA- 2014/06/15 06:00
CRDT- 2013/10/23 06:00
PHST- 2012/07/05 00:00 [received]
PHST- 2013/03/11 00:00 [revised]
PHST- 2013/10/23 06:00 [entrez]
PHST- 2013/10/23 06:00 [pubmed]
PHST- 2014/06/15 06:00 [medline]
AID - S1734-1140(13)71077-6 [pii]
AID - 10.1016/s1734-1140(13)71077-6 [doi]
PST - ppublish
SO  - Pharmacol Rep. 2013;65(4):960-9. doi: 10.1016/s1734-1140(13)71077-6.