title: Mannose-binding lectin in obesity with different degrees of metabolic syndrome abnormalities: association with atherogenic and metabolic traits.
abstract: OBJECTIVE
  In subjects with metabolic syndrome (MetS) endothelial dysfunction is a very consistent finding. Processes leading to endothelial dysfunction and atherosclerosis involve the altered control of subclinical inflammation by innate immune defenses that possibly include mannose-binding lectin (MBL). We investigated the associations of MBL with traits of MetS and early atherosclerosis in obese subjects before and after marked weight reduction.
  
  
  METHODS
  In a prospective longitudinal study, MBL concentrations of 96 severely obese subjects with and without MetS (Ø BMI with MetS 41.0±7.9 kg/m(2), Ø BMI without MetS 39.4±7.7 kg/m(2) were examined in association with markers of insulin resistance, dyslipidemia, adipokines, and subclinical atherosclerosis before and after marked weight loss (Ø weight loss 20±8 kg after 3 months of participation in a standardized weight reduction program), in addition to the study of 25 seemingly healthy lean subjects (BMI 20-25 kg/m(2).
  
  
  RESULTS
  MBL concentrations did not differ between healthy lean and severely obese subjects independently of the presence of metabolic abnormalities. In severely obese subjects there was no significant difference concerning the cardiovascular risk profile, apolipoproteins, inflammatory and metabolic parameters, and markers of endothelial dysfunction and atherosclerosis between subjects with functional MBL deficienct (MBL<778 ng/mL) and MBL sufficient (MBL≥778 ng/mL) obesity. Marked weight loss did not influence MBL levels.
  
  
  CONCLUSIONS
  Our findings suggest that plasma levels of MBL did not differ between healthy lean and severely obese subjects. MBL did not affect cardiovascular risk factors, or markers of endothelial dysfunction and early atherosclerosis in severely obese patients before and after marked weight loss.
authors.affiliation: Clinic for Internal Medicine II, University Medical Centre, Regensburg, Germany.
authors.forename: Christina
authors.initials: C
authors.lastname: Strack
authors.forename: Andrea
authors.initials: A
authors.lastname: Baessler
authors.forename: Florian
authors.initials: F
authors.lastname: Wagner
authors.forename: Janine
authors.initials: J
authors.lastname: Bruxmeier
authors.forename: Oleg
authors.initials: O
authors.lastname: Yaroslavskii
authors.forename: Elena
authors.initials: E
authors.lastname: Rousseva
authors.forename: Thomas
authors.initials: T
authors.lastname: Loew
authors.forename: Gunter
authors.initials: G
authors.lastname: Riegger
authors.forename: Gerd
authors.initials: G
authors.lastname: Schmitz
authors.forename: Marcus
authors.initials: M
authors.lastname: Fischer
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology* / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology* / Q000473:pathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008137:Longitudinal Studies; D008297:Male; D037241:Mannose-Binding Lectins / Q000097:blood*; D024821:Metabolic Syndrome / Q000097:blood / Q000209:etiology* / Q000473:pathology; D009765:Obesity / Q000097:blood / Q000150:complications* / Q000473:pathology; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D015431:Weight Loss; D061217:Weight Reduction Programs
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D037241:Mannose-Binding Lectins