title: Bariatric surgery cannot prevent tryptophan depletion due to chronic immune activation in morbidly obese patients.
abstract: BACKGROUND
  Increased activity of the immuno-modulatory enzyme indoleamine-2,3-dioxygenase (IDO) during immune activation, results in tryptophan depletion. Tryptophan metabolic changes reduce serotonin production and cause mood disturbances, depression, and impaired satiety, ultimately leading to increased food intake and obesity. Bariatric surgery significantly diminishes immune mediators by substantial weight reduction. We examined IDO-mediated tryptophan-catabolism in morbidly obese patients compared to lean individuals.
  
  
  METHODS
  Serum concentrations of kynurenine and tryptophan, calculated kynurenine to tryptophan ratios (kyn trp-1) as an indirect estimate of IDO activity, and neopterin levels reflecting IFN-gamma mediated immune activation, were assessed before and after bariatric surgery. The study population included 22 morbidly obese individuals and 20 normal-weight volunteers.
  
  
  RESULTS
  Median weight loss after 24.4+/-5.1 months was 40.6 kg resulting in a reduction of BMI from 44.1 kg/m(2) to 29.9 kg/m(2) (P<0.001). Preoperative kyn trp-1 in morbidly obese patients was significantly increased compared to the control group (41.6+/-20.1 mmol/mol vs 26.5+/-5.1 mmol/mol; P<0.001). Postoperative weight reduction did not lead to normalization of kyn trp-1 (37.9+/-14.0 mmol/mol). As a consequence, tryptophan levels were significantly lower in morbidly obese patients (pre-: 51.5+/-9.2 micromol L(-1) and postoperatively: 46.9+/-7.6 micromol L(-1)) when compared with those of normal-weight controls (64.8+/-9.5 micromol L(-1); P<0.001). In addition, neopterin levels were elevated in the study population pre- and postoperatively compared to normal-weight volunteers (both P<0.001).
  
  
  CONCLUSIONS
  Tryptophan depletion in morbidly obese patients is due to chronic immune activation and persists in spite of significant weight reduction following bariatric surgery. This might thereby be responsible for diminished serotonin functions, leading to unchanged satiety dysregulation and a reward-deficiency-syndrome.
authors: Department of General and Transplant Surgery, Ludwig Boltzmann Institute for AIDS-Research, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria.
authors: Gerald
authors: G
authors: Brandacher
authors: Christiana
authors: C
authors: Winkler
authors: Franz
authors: F
authors: Aigner
authors: Hubert
authors: H
authors: Schwelberger
authors: Katrin
authors: K
authors: Schroecksnadel
authors: Raimund
authors: R
authors: Margreiter
authors: Dietmar
authors: D
authors: Fuchs
authors: Helmut G
authors: HG
authors: Weiss