title: Serum visfatin is differentially regulated by insulin and free Fatty acids in healthy men.
abstract: BACKGROUND
  Serum visfatin is elevated in insulin-resistant states, ie, obesity, type 2 diabetes mellitus, and polycystic ovary syndrome, thus linking visfatin with the pathogenesis of insulin resistance.
  
  
  OBJECTIVE
  Our objective was to evaluate the effect of hyperinsulinemia and the acute elevation of free fatty acids (FFAs) on serum visfatin in humans.
  
  
  METHODS
  We estimated serum visfatin during hyperinsulinemia and the insulin-resistant conditions caused by an acute elevation of FFAs in 19 healthy male volunteers (mean age, 25 ± 7 years; body mass index, 26 ± 4 kg/m(2)) at a university hospital.
  
  
  METHODS
  Intervention included a 6-hour euglycemic-hyperinsulinemic clamp without and with Intralipid/heparin infusion.
  
  
  METHODS
  Measurements were made of serum visfatin at baseline and at 2 and 6 hours during both clamp studies.
  
  
  RESULTS
  Hyperinsulinemia resulted in a significant decrease in serum visfatin concentration (P = .043). Concomitant Intralipid/heparin infusion, which caused a reduction of insulin sensitivity by 40% (P < .0001), resulted in a marked increase in serum visfatin (P < .0001), which was already observed after 2 hours of FFAs increase (P < .0001). Serum visfatin during the clamp study after 2 and 6 hours of Intralipid/heparin infusion was significantly higher than respective values during the clamp study without the elevation of FFAs (both P < .0001). The increase in serum visfatin during Intralipid/heparin infusion was positively related to body weight (r = 0.54, P = .016) and γ-glutamyltransferase activity (r = 0.56, P = .011).
  
  
  CONCLUSIONS
  Serum visfatin is differentially regulated by insulin and FFAs. One might hypothesize that the induction of insulin resistance by FFAs suppresses insulin inhibition of visfatin secretion, resulting in a serum visfatin increase in insulin-resistant conditions.
authors.affiliation: Department of Endocrinology, Diabetology, and Internal Medicine, Medical University of Bialystok, M.C. Sklodowskiej 24a, 15-276 Bialystok, Poland.
authors.forename: Irina
authors.initials: I
authors.lastname: Kowalska
authors.forename: Monika
authors.initials: M
authors.lastname: Karczewska-Kupczewska
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Adamska
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Nikolajuk
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Otziomek
authors.forename: Marek
authors.initials: M
authors.lastname: Straczkowski
mesh_terms: D000328:Adult; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D015309:Glucose Clamp Technique; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*
chemical_list: D005230:Fatty Acids, Nonesterified; D007328:Insulin; D054409:Nicotinamide Phosphoribosyltransferase