title: APOH is increased in the plasma and liver of type 2 diabetic patients with metabolic syndrome.
abstract: OBJECTIVE
  To assess the association of APOH with metabolic and cardiovascular risk markers in type 2 diabetic patients.
  
  
  METHODS
  In a cohort of 169 type 2 diabetic subjects, plasma levels of APOH, antibodies anti-APOH, lipoprotein subfractions, oxidation, inflammatory and insulin resistance markers and the Trp316Ser and Val247Leu variations in the APOH gene were analyzed. Apo H mRNA levels and protein content were measured in hepatic and adipose tissue (subcutaneous and visceral) samples obtained during bariatric surgery from three diabetics who fulfilled metabolic syndrome (MS) criteria and three non-diabetic, non-MS.
  
  
  RESULTS
  APOH plasma levels were significantly associated with triglycerides (p<0.001), all the components of triglyceride-rich lipoproteins (p<0.001) and RBP4 (p<0.001) levels. APOH was higher in type 2 diabetic patients with MS (p=0.003) and with clinical evidence of macrovascular disease (p=0.012). The Trp316Ser and Val247Leu APOH gene variants did not modulate APOH plasma values. Neither Apo H mRNA nor protein was detected in the adipose tissue. Liver from patients with diabetes and MS showed a significant increase of both Apo H mRNA and protein respect to the non-diabetic, non-MS patients.
  
  
  CONCLUSIONS
  APOH plasma concentrations are strongly associated to MS alterations and vascular disease in type 2 diabetic patients and could be considered as a clinical marker of cardiovascular risk. The enhanced APOH levels in these patients are due to an increased liver synthesis. If APOH plays a major causal role in macrovascular lesions associated to diabetes and MS need further studies.
authors.affiliation: Department of Internal Medicine and Research Unit on Lipids and Atherosclerosis, Sant Joan University Hospital, Rovira & Virgili University, Reus, Spain.
authors.forename: Antoni
authors.initials: A
authors.lastname: Castro
authors.forename: Iolanda
authors.initials: I
authors.lastname: Lázaro
authors.forename: David M
authors.initials: DM
authors.lastname: Selva
authors.forename: Ela
authors.initials: E
authors.lastname: Céspedes
authors.forename: Josefa
authors.initials: J
authors.lastname: Girona
authors.lastname: NúriaPlana
authors.forename: Montse
authors.initials: M
authors.lastname: Guardiola
authors.forename: Anna
authors.initials: A
authors.lastname: Cabré
authors.forename: Rafael
authors.initials: R
authors.lastname: Simó
authors.forename: Lluís
authors.initials: L
authors.lastname: Masana
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000175:diagnosis* / Q000453:epidemiology / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism*; D005260:Female; D006801:Humans; D008099:Liver / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000378:metabolism*; D008875:Middle Aged; D012306:Risk; D053482:beta 2-Glycoprotein I / Q000097:blood / Q000235:genetics / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D053482:beta 2-Glycoprotein I