title: Roux-en-Y gastric bypass alters tumor necrosis factor-α but not adiponectin signaling in immediate postoperative period in obese rats.
abstract: BACKGROUND
  Adiponectin has anti-inflammatory properties and is increased with weight loss. Tumor necrosis factor (TNF)-α is a pro-inflammatory cytokine that negatively regulates adiponectin. Previously, we have demonstrated that Roux-en-Y gastric bypass (RYGB) induces weight loss and improves steatosis in obese rats. We hypothesized that RYGB would alter the interplay of TNF-α and adiponectin signaling in the postoperative period.
  
  
  METHODS
  Obese Sprague-Dawley male rats that had undergone RYGB (n = 5) or sham (n = 4) were euthanatized at 9 weeks postoperatively. The adiponectin levels from serial serum samples were measured by enzyme-linked immunosorbent assay. Adiponectin, adiponectin receptor 2, and TNF-α mRNA from adipose and liver samples were quantified by reverse transcriptase-polymerase chain reaction. Data are presented as mean ± standard deviation; using a t test, P <.05 was significant.
  
  
  RESULTS
  RYGB did not change the serum adiponectin, adipose tissue adiponectin mRNA, or hepatic adiponectin receptor 2 levels compared with the levels in the sham-operated rats (P >.05). However, the TNF-α mRNA levels had decreased in the adipose tissue (P >.05) but remained unchanged in the liver compared with the sham controls (P >.05).
  
  
  CONCLUSIONS
  Surgically-induced weight loss in a rat model of RYGB did not increase adiponectin signaling in the immediate postoperative period but was associated with decreased pro-inflammatory signaling in the adipose tissue. During this period, pro-inflammatory signaling might play a more important role than adiponectin. Additional studies with longer follow-up are necessary to determine whether adiponectin plays a role in weight loss and improvement of steatosis after RYGB.
authors.affiliation: Department of Surgery, James A. Haley Veterans Affairs Medical Center, University of South Florida, Tampa, Florida, USA.
authors.forename: Drew A
authors.initials: DA
authors.lastname: Rideout
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Peng
authors.forename: Steven S
authors.initials: SS
authors.lastname: Rakita
authors.forename: Karan
authors.initials: K
authors.lastname: Desai
authors.forename: William R
authors.initials: WR
authors.lastname: Gower
authors.forename: Min
authors.initials: M
authors.lastname: You
authors.forename: Michel M
authors.initials: MM
authors.lastname: Murr
mesh_terms: D052242:Adiponectin / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D015390:Gastric Bypass; D007249:Inflammation / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000378:metabolism* / Q000601:surgery*; D011184:Postoperative Period; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D054419:Receptors, Adiponectin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
chemical_list: D052242:Adiponectin; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; D014409:Tumor Necrosis Factor-alpha; C506573:adiponectin receptor 2, rat