title: Increase of osteopontin plasma concentrations after bariatric surgery independent from inflammation and insulin resistance.
abstract: BACKGROUND
  Osteopontin (OPN) is a multifunctional matrix glycoprotein associated with bone metabolism and has been linked to chronic inflammation, insulin resistance, and atherosclerosis. Diet-induced weight loss decreases elevated OPN concentrations in obese patients. The aim of the current study was to investigate the role of OPN after bariatric surgery, where not only improvements of chronic inflammation, insulin resistance and comorbidities, but also malabsorption and altered bone metabolism have been reported.
  
  
  METHODS
  OPN plasma concentrations were determined in 31 morbidly obese patients (5 men, 26 women, BMI 46.2+/-7.1 kg/m2, age 41+/-11 years; mean+/-SD) before and 18 months after bariatric surgery, together with parameters of bone metabolism and inflammation.
  
  
  RESULTS
  OPN concentrations increased by +20.3+/-26.6 ng/ml (mean+/-SD, p<0.01), concomitant to a weight loss of -38+/-22 kg, and a decrease in BMI by -13.1+/-7.7 kg/m2 (both p<0.01). HOMA-index improved from 5.2+/-3.4 to 1.5+/-1.0 (p<0.01). Calcium concentrations slightly decreased, and phosphate increased (-0.06+/-0.13 mmol/l and +0.08+/-0.16 mmol/l, respectively; both p<0.05), while 25-OH-Vitamin D3 remained unchanged and PTH tended to increase (+5.1+/-14.0 pg/ml, p=0.054). Monocyte chemoattractant protein 1 and interleukin 18 were significantly decreased and associated with HOMA both before and after bariatric surgery. DeltaOPN was correlated with DeltaPTH, but not with other parameters.
  
  
  CONCLUSIONS
  OPN plasma concentrations increased concomitant to weight loss after bariatric surgery, which was independent from an improvement of insulin sensitivity and a decrease of inflammatory markers. Further studies are needed to differentiate whether these changes in bone metabolism after bariatric surgery are secondary to calcium deficiency or an adaptation to weight loss.
authors.affiliation: Department of Internal Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030, and Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. georg.schaller@wienkav.at
authors.forename: Georg
authors.initials: G
authors.lastname: Schaller
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Aso
authors.forename: Gerit-Holger
authors.initials: GH
authors.lastname: Schernthaner
authors.forename: Hans-Peter
authors.initials: HP
authors.lastname: Kopp
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Inukai
authors.forename: Stefan
authors.initials: S
authors.lastname: Kriwanek
authors.forename: Guntram
authors.initials: G
authors.lastname: Schernthaner
mesh_terms: D000328:Adult; D015992:Body Mass Index; D016723:Bone Remodeling / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000097:blood; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D020382:Interleukin-18 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000097:blood* / Q000601:surgery*; D053495:Osteopontin / Q000097:blood*; D016896:Treatment Outcome; D015431:Weight Loss / Q000502:physiology
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D020382:Interleukin-18; D053495:Osteopontin; D002097:C-Reactive Protein