title: Role of HDL cholesterol and estimates of HDL particle composition in future development of type 2 diabetes in the general population: the PREVEND study.
abstract: OBJECTIVE
  High-density lipoproteins (HDLs) may directly stimulate β-cell function and glucose metabolism. We determined the relationships of fasting high-density lipoprotein cholesterol (HDL-C), plasma apolipoprotein (apo) A-I and apoA-II, and HDL-C-to-apoA-I and HDL-C-to-apoA-II ratios, as estimates of HDL particle composition, with incident type 2 diabetes mellitus.
  
  
  METHODS
  A prospective study was carried out in the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort after exclusion of subjects with diabetes at baseline (n = 6820; age, 28-75 years). The association of HDL-related variables with incident type 2 diabetes was determined by multivariate logistic regression analyses.
  
  
  RESULTS
  After a median follow-up of 7.7 years, 394 incident cases of type 2 diabetes mellitus were ascertained (5.8%). After adjustment for age, sex, family history of diabetes, body mass index, hypertension, alcohol, and smoking, odd ratios (ORs) for diabetes were 0.55 (95% confidence interval [CI], 0.47-0.64; P < .001), 0.81 (0.71-0.93; P = .002), 0.02 (0.01-0.06; P < .001), and 0.03 (0.01-0.060; P < .001) per 1-SD increase in HDL-C and apoA-I and in the HDL-C-to-apoA-I and the HDL-C-to-apoA-II ratios, respectively. In contrast, apoA-II was not related to incident diabetes (OR = 1.02; 95% CI, 0.90-1.16; P=0.71). The relationships of HDL-C and the ratios of HDL-C to apoA-I and HDL-C to apoA-II remained significant after further adjustment for baseline glucose and triglycerides (OR(HDL) = 0.74 [95% CI, 0.61-0.88], OR(HDL/APO A-I) = 0.14 [0.04-0.44], and OR(HDL/APOA-II) = 0.12 [0.04-0.36]; all P ≤ .001).
  
  
  CONCLUSIONS
  Higher HDL-C, as well as higher HDL-C-to-apoA-I and HDL-C-to-apoA-II ratios are strongly and independently related to a lower risk of future type 2 diabetes.
authors.affiliation: Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen 9700 RB, The Netherlands.
authors.forename: Ali
authors.initials: A
authors.lastname: Abbasi
authors.forename: Eva
authors.initials: E
authors.lastname: Corpeleijn
authors.forename: Ron T
authors.initials: RT
authors.lastname: Gansevoort
authors.forename: Rijk O B
authors.initials: RO
authors.lastname: Gans
authors.forename: Hans L
authors.initials: HL
authors.lastname: Hillege
authors.forename: Ronald P
authors.initials: RP
authors.lastname: Stolk
authors.forename: Gerjan
authors.initials: G
authors.lastname: Navis
authors.forename: Stephan J L
authors.initials: SJ
authors.lastname: Bakker
authors.forename: Robin P F
authors.initials: RP
authors.lastname: Dullaart
mesh_terms: D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000032:analysis; D016633:Apolipoprotein A-II / Q000032:analysis; D008076:Cholesterol, HDL / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000209:etiology*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000517:prevention & control; D008075:Lipoproteins, HDL / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012306:Risk
chemical_list: C505693:APOA1 protein, human; C115794:APOA2 protein, human; D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D008076:Cholesterol, HDL; D008075:Lipoproteins, HDL