title: Plasma lipopolysaccharide is closely associated with glycemic control and abdominal obesity: evidence from bariatric surgery.
abstract: OBJECTIVE
  It is of vital importance to elucidate the triggering factors of obesity and type 2 diabetes to improve patient care. Bariatric surgery has been shown to prevent and even cure diabetes, but the mechanism is unknown. Elevated levels of lipopolysaccharide (LPS) predict incident diabetes, but the sources of LPS are not clarified. The objective of the current study was to evaluate the potential impact of plasma LPS on abdominal obesity and glycemic control in subjects undergoing bariatric surgery.
  
  
  METHODS
  This was a prospective observational study involving a consecutive sample of 49 obese subjects undergoing bariatric surgery and 17 controls. Main assessments were plasma LPS, HbA1c, adipose tissue volumes (computed tomography), and quantified bacterial DNA in adipose tissue compartments.
  
  
  RESULTS
  Plasma levels of LPS were elevated in obese individuals compared with controls (P < 0.001) and were reduced after bariatric surgery (P = 0.010). LPS levels were closely correlated with HbA1c (r = 0.56; P = 0.001) and intra-abdominal fat volumes (r = 0.61; P < 0.001), but only moderately correlated with subcutaneous fat volumes (r = 0.33; P = 0.038). Moreover, there was a decreasing gradient (twofold) in bacterial DNA levels going from mesenteric via omental to subcutaneous adipose tissue compartments (P = 0.041). Finally, reduced LPS levels after bariatric surgery were directly correlated with a reduction in HbA1c (r = 0.85; P < 0.001).
  
  
  CONCLUSIONS
  Our findings support a hypothesis of translocated gut bacteria as a potential trigger of obesity and diabetes, and suggest that the antidiabetic effects of bariatric surgery might be mechanistically linked to, and even the result of, a reduction in plasma levels of LPS.
authors.affiliation: Corresponding author: Marius Trøseid, troseid@hotmail.com.
authors.forename: Marius
authors.initials: M
authors.lastname: Trøseid
authors.forename: Torunn K
authors.initials: TK
authors.lastname: Nestvold
authors.forename: Knut
authors.initials: K
authors.lastname: Rudi
authors.forename: Hanne
authors.initials: H
authors.lastname: Thoresen
authors.forename: Erik W
authors.initials: EW
authors.lastname: Nielsen
authors.forename: Knut T
authors.initials: KT
authors.lastname: Lappegård
mesh_terms: D000328:Adult; D050110:Bariatric Surgery; D001786:Blood Glucose; D004269:DNA, Bacterial / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000382:microbiology / Q000517:prevention & control; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D050152:Intra-Abdominal Fat / Q000000981:diagnostic imaging / Q000382:microbiology / Q000601:surgery; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood*; D008297:Male; D008875:Middle Aged; D056128:Obesity, Abdominal / Q000097:blood / Q000382:microbiology* / Q000601:surgery*; D009852:Omentum / Q000382:microbiology / Q000601:surgery; D011446:Prospective Studies; D050151:Subcutaneous Fat / Q000000981:diagnostic imaging / Q000382:microbiology / Q000601:surgery; D014057:Tomography, X-Ray Computed
chemical_list: D001786:Blood Glucose; D004269:DNA, Bacterial; D006442:Glycated Hemoglobin; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; C517652:hemoglobin A1c protein, human