title: Extended-release niacin decreases serum fetuin-A concentrations in individuals with metabolic syndrome.
abstract: BACKGROUND
  Fetuin-A, a liver-secreted phosphoprotein and physiological inhibitor of insulin receptor tyrosine kinase, is associated with insulin resistance, metabolic syndrome (MetS), and an increased risk for type 2 diabetes. However, studies on the modulation of circulating levels of fetuin-A are limited. The goal of this study was to determine the effect of niacin administration on serum total- and phosphorylated fetuin-A (phosphofetuin-A) concentrations in individuals with MetS and correlate with changes in serum lipids, insulin sensitivity, and markers of inflammation.
  
  
  METHODS
  Fifteen sedentary, obese, male participants, who met the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria for MetS, were treated with extended-release niacin (Niaspan) for 6 weeks. Blood samples were obtained before and after treatment with niacin.
  
  
  RESULTS
  Serum fetuin-A and phosphofetuin-A concentrations were decreased following niacin administration (p < 0.005). Changes in fetuin-A concentrations were correlated with changes in triglyceride (r = 0.62, p = 0.01) and C-reactive protein (CRP) concentrations (r = 0.58, p < 0.05) after niacin treatment. Changes in high-density lipoproteins (HDL)-cholesterol following niacin intervention were negatively correlated with changes in serum fetuin-A (p < 0.05) and phosphofetuin-A concentrations (p < 0.05). Serum cortisol levels were significantly elevated after niacin administration.
  
  
  CONCLUSIONS
  Niacin treatment lowers serum total- and phosphofetuin-A concentrations in individuals with MetS, and these changes correlate with the beneficial changes in serum lipids. Because niacin is known to induce insulin resistance, these findings suggest that fetuin-A may not be a mediator of niacin-induced insulin resistance but it may blunt the insulin resistance induced by niacin by decreasing its circulating concentrations.
authors.affiliation: Department of Nutrition and Food Science, Auburn University, Auburn, AL 36849, USA.
authors.forename: Shalini V
authors.initials: SV
authors.lastname: Kaushik
authors.forename: Eric P
authors.initials: EP
authors.lastname: Plaisance
authors.forename: Teayoun
authors.initials: T
authors.lastname: Kim
authors.forename: Edmond Y
authors.initials: EY
authors.lastname: Huang
authors.forename: A Jack
authors.initials: AJ
authors.lastname: Mahurin
authors.forename: Peter W
authors.initials: PW
authors.lastname: Grandjean
authors.forename: Suresh T
authors.initials: ST
authors.lastname: Mathews
mesh_terms: D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000032:analysis / Q000187:drug effects*; D002097:C-Reactive Protein / Q000032:analysis / Q000187:drug effects; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D003692:Delayed-Action Preparations / Q000008:administration & dosage*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood*; D008875:Middle Aged; D009525:Niacin / Q000008:administration & dosage*; D009765:Obesity / Q000097:blood; D010750:Phosphoproteins / Q000032:analysis / Q000187:drug effects; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D001798:Blood Proteins; D008076:Cholesterol, HDL; D003692:Delayed-Action Preparations; D010750:Phosphoproteins; D014280:Triglycerides; D060749:alpha-2-HS-Glycoprotein; D009525:Niacin; D002097:C-Reactive Protein