title: Preoperative diet impacts the adipose tissue response to surgical trauma.
abstract: BACKGROUND
  Short-term changes in preoperative nutrition can have profound effects on surgery-related outcomes such as ischemia/reperfusion injury in preclinical models. Dietary interventions that lend protection against stress in animal models (eg, fasting, dietary restriction [DR]) impact adipose tissue quality/quantity. Adipose tissue holds high surgical relevance because of its anatomic location and large tissue volume, and it is ubiquitously traumatized during surgery. Yet the response of adipose tissue to trauma under clinically relevant circumstances including dietary status remains poorly defined. We hypothesized that preoperative diet alters the adipose tissue response to surgical trauma.
  
  
  METHODS
  A novel mouse model of adipose tissue surgical trauma was employed. Dietary conditions (diet-induced obesity [DIO], preoperative DR) were modulated before application of surgical adipose tissue trauma in the context of clinically common scenarios (different ages, simulated bacterial wound contamination). Local/distant adipose tissue phenotypic responses were measured as represented by gene expression of inflammatory, tissue remodeling/growth, and metabolic markers.
  
  
  RESULTS
  Surgical trauma had a profound effect on adipose tissue phenotype at the site of trauma. Milder but significant distal effects on non-traumatized adipose tissue were also observed. DIO exacerbated the inflammatory aspects of this response, and preoperative DR tended to reverse these changes. Age and lipopolysaccharide (LPS)-simulated bacterial contamination also impacted the adipose tissue response to trauma, with young adult animals and LPS treatment exacerbating the proinflammatory response.
  
  
  CONCLUSIONS
  Surgical trauma dramatically impacts both local and distal adipose tissue biology. Short-term preoperative DR may offer a strategy to attenuate this response.
authors.affiliation: Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Binh
authors.initials: B
authors.lastname: Nguyen
authors.forename: Ming
authors.initials: M
authors.lastname: Tao
authors.forename: Peng
authors.initials: P
authors.lastname: Yu
authors.forename: Christine
authors.initials: C
authors.lastname: Mauro
authors.forename: Michael A
authors.initials: MA
authors.lastname: Seidman
authors.forename: Yaoyu E
authors.initials: YE
authors.lastname: Wang
authors.forename: James
authors.initials: J
authors.lastname: Mitchell
authors.forename: C Keith
authors.initials: CK
authors.lastname: Ozaki
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D000367:Age Factors; D000818:Animals; D031204:Caloric Restriction; D004032:Diet; D059305:Diet, High-Fat; D002149:Energy Intake; D015870:Gene Expression; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011300:Preoperative Care; D025341:Principal Component Analysis
chemical_list: D018836:Inflammation Mediators