title: Impaired fasting glucose and impaired glucose tolerance have distinct lipoprotein and apolipoprotein changes: the insulin resistance atherosclerosis study.
abstract: BACKGROUND
  Cardiovascular risk is increased in individuals with impaired glucose tolerance (IGT) and impaired fasting glucose (IFG); however, those with IGT appear to be at greater risk. Lipoprotein abnormalities occur also in the prediabetic state.
  
  
  OBJECTIVE
  The authors examined lipoprotein composition in IGT and IFG.
  
  
  METHODS
  Cross-sectional analysis of a large epidemiological study was done.
  
  
  METHODS
  The Insulin Resistance Atherosclerosis Study had a total of 1107 participants.
  
  
  METHODS
  Lipoproteins and apolipoproteins were measured by conventional methods and lipoprotein composition by nuclear magnetic resonance spectroscopy.
  
  
  RESULTS
  Compared with normal glucose tolerance, apolipoprotein B (105.2 vs 99.8 mg/dL, P < .05) was high in isolated IFG, triglyceride (1.48 vs 1.16 mmol/L, P < .001) was high in isolated IGT, and high-density lipoprotein cholesterol was low in combined IFG/IGT (1.12 vs 1.26 mmol/L, P < .001). Nuclear magnetic resonance spectroscopy revealed additional changes: increased total low-density lipoprotein (LDL) particles (1190 vs 1096 nmol/L, P < .01) in isolated IFG; increased large very-low-density lipoprotein (3.61 vs 2.47 nmol/L, P < .01) and small LDL subclass particles (665 vs 541 nmol/L, P < .05) and decreased large LDL subclass particles (447 vs 513 nmol/L, P < .01) in isolated IGT; and decreased large high-density lipoprotein subclass particles in combined IFG/IGT (4.24 vs 5.39 μmol/L, P < .001).
  
  
  CONCLUSIONS
  Isolated IFG is characterized by increased apolipoprotein B and total LDL particles, whereas isolated IGT is associated with increased triglycerides, large very-low-density lipoprotein subclass particles, and structural remodeling of LDL particles. These results may help to explain differences in cardiovascular disease risk in the prediabetic state.
authors: Division of Clinical Epidemiology, Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229, USA. lorenzo@uthscsa.edu
authors: Carlos
authors: C
authors: Lorenzo
authors: Sara
authors: S
authors: Hartnett
authors: Anthony J
authors: AJ
authors: Hanley
authors: Marian J
authors: MJ
authors: Rewers
authors: Lynne E
authors: LE
authors: Wagenknecht
authors: Andrew J
authors: AJ
authors: Karter
authors: Steven M
authors: SM
authors: Haffner
mesh_terms: D000328:Adult; D000368:Aged; D001053:Apolipoproteins / Q000097:blood* / Q000378:metabolism; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005215:Fasting / Q000097:blood* / Q000378:metabolism; D005260:Female; D018149:Glucose Intolerance / Q000097:blood* / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008074:Lipoproteins / Q000097:blood* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011236:Prediabetic State / Q000097:blood / Q000378:metabolism
chemical_list: D001053:Apolipoproteins; D001786:Blood Glucose; D008074:Lipoproteins