title: Impact of diabetes mellitus on the relationships between iron-, inflammatory- and oxidative stress status.
abstract: BACKGROUND
  Diabetes is an inflammatory condition associated with iron abnormalities and increased oxidative damage. We aimed to investigate how diabetes affects the interrelationships between these pathogenic mechanisms.
  
  
  METHODS
  Glycaemic control, serum iron, proteins involved in iron homeostasis, global antioxidant capacity and levels of antioxidants and peroxidation products were measured in 39 type 1 and 67 type 2 diabetic patients and 100 control subjects.
  
  
  RESULTS
  Although serum iron was lower in diabetes, serum ferritin was elevated in type 2 diabetes (p = 0.02). This increase was not related to inflammation (C-reactive protein) but inversely correlated with soluble transferrin receptors (r = - 0.38, p = 0.002). Haptoglobin was higher in both type 1 and type 2 diabetes (p < 0.001) and haemopexin was higher in type 2 diabetes (p < 0.001). The relation between C-reactive protein and haemopexin was lost in type 2 diabetes (r = 0.15, p = 0.27 vs r = 0.63, p < 0.001 in type 1 diabetes and r = 0.36, p = 0.001 in controls). Haemopexin levels were independently determined by triacylglycerol (R(2) = 0.43) and the diabetic state (R(2) = 0.13). Regarding oxidative stress status, lower antioxidant concentrations were found for retinol and uric acid in type 1 diabetes, alpha-tocopherol and ascorbate in type 2 diabetes and protein thiols in both types. These decreases were partially explained by metabolic-, inflammatory- and iron alterations. An additional independent effect of the diabetic state on the oxidative stress status could be identified (R(2) = 0.5-0.14).
  
  
  CONCLUSIONS
  Circulating proteins, body iron stores, inflammation, oxidative stress and their interrelationships are abnormal in patients with diabetes and differ between type 1 and type 2 diabetes.
authors.affiliation: Laboratory of Endocrinology, Antwerp Metabolic Research Unit, University of Antwerp T4.37, Universiteitsplein 1, B-2610 Wilrijk-Antwerp, Belgium. ann.vancampenhout@ua.ac.be
authors.forename: Ann
authors.initials: A
authors.lastname: Van Campenhout
authors.forename: Christel
authors.initials: C
authors.lastname: Van Campenhout
authors.forename: Albert R
authors.initials: AR
authors.lastname: Lagrou
authors.forename: Pascale
authors.initials: P
authors.lastname: Abrams
authors.forename: Greta
authors.initials: G
authors.lastname: Moorkens
authors.forename: Luc
authors.initials: L
authors.lastname: Van Gaal
authors.forename: Begoña
authors.initials: B
authors.lastname: Manuel-y-Keenoy
mesh_terms: D000328:Adult; D000368:Aged; D000941:Antigens / Q000032:analysis; D000975:Antioxidants / Q000032:analysis; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D002570:Ceruloplasmin / Q000032:analysis; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D005260:Female; D005293:Ferritins / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D006242:Haptoglobins / Q000032:analysis; D006466:Hemopexin / Q000032:analysis; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007501:Iron / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D011990:Receptors, Transferrin / Q000097:blood; D014168:Transferrin / Q000032:analysis; D014841:von Willebrand Factor / Q000276:immunology
chemical_list: D000941:Antigens; D000975:Antioxidants; D001786:Blood Glucose; D006242:Haptoglobins; D011990:Receptors, Transferrin; D014168:Transferrin; C029417:Von Willebrand antigen; D014841:von Willebrand Factor; D005340:Fibrinogen; D002097:C-Reactive Protein; D005293:Ferritins; D006466:Hemopexin; D007501:Iron; D002570:Ceruloplasmin