title: Features of the metabolic syndrome predict higher risk of diabetes and impaired glucose tolerance: a prospective study in Mauritius.
abstract: OBJECTIVE
  To assess the independent and joint effects of the components of the metabolic syndrome, including leptin, which is a recently proposed addition to this syndrome, in predicting the cumulative incidence of impaired glucose tolerance (IGT) and diabetes among individuals with normal glucose tolerance.
  
  
  METHODS
  This prospective study involved 2,605 residents of Mauritius with normal glucose tolerance who were followed for 5 years for IGT or diabetes onset in relation to total and regional adiposity (BMI, waist-to-hip ratio [WHR]), fasting and 2-h 75-g oral glucose load glucose and insulin, total and HDL cholesterol, blood pressure, serum uric acid, triglyceride, and leptin levels.
  
  
  RESULTS
  A multivariate logistic regression model adjusted for age, sex, ethnicity, and diabetes family history showed a significantly higher linear increase in risk of IGT and diabetes in association with the following variables only: fasting glucose (odds ratio 1.89 [95% CI 1.51-2.34]), 2-h glucose (1.68 [1.50-1.88]), WHR (1.30 [1.10-1.52]), BMI (1.04 [1.00-1.08]), and serum uric acid (1.37 [1.20-1.57]). However, a nonlinear increase was seen with serum triglyceride and plasma leptin concentrations. No risk factors resulted in joint effects that were greater than expected from combining individual effects.
  
  
  CONCLUSIONS
  Metabolic syndrome features independently predict a higher risk of diabetes or IGT in normoglycemic subjects but in combination confer no higher-than-expected risk of these outcomes. At higher concentrations of triglycerides and leptin, risk plateaus and even declines slightly.
authors.affiliation: International Diabetes Institute, Melbourne, Victoria, Australia. eboyko@u.washington.edu
authors.forename: E J
authors.initials: EJ
authors.lastname: Boyko
authors.forename: M
authors.initials: M
authors.lastname: de Courten
authors.forename: P Z
authors.initials: PZ
authors.lastname: Zimmet
authors.forename: P
authors.initials: P
authors.lastname: Chitson
authors.forename: J
authors.initials: J
authors.lastname: Tuomilehto
authors.forename: K G
authors.initials: KG
authors.lastname: Alberti
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology*; D005006:Ethnicity; D005260:Female; D018149:Glucose Intolerance / Q000453:epidemiology*; D005951:Glucose Tolerance Test; D006801:Humans; D006949:Hyperlipidemias / Q000453:epidemiology*; D006973:Hypertension / Q000453:epidemiology*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood*; D008137:Longitudinal Studies; D008297:Male; D008436:Mauritius / Q000453:epidemiology; D008875:Middle Aged; D015999:Multivariate Analysis; D011446:Prospective Studies; D044469:Racial Groups; D012044:Regression Analysis; D012307:Risk Factors; D013577:Syndrome; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020738:Leptin