title: Niacin treatment of the atherogenic lipid profile and Lp(a) in diabetes.
abstract: OBJECTIVE
  We tested the hypotheses that niacin is effective for the separate treatments of abnormalities of LDL particle size, HDL2 percentage and Lp(a) without potential negative effects on glycated haemoglobin.
  
  
  METHODS
  The atherogenic lipid profile lipids, such as triglycerides, small, dense LDL cholesterol (LDLc) particle mass, LDL particle size, total HDLc and HDL2 percentage as well as Lp(a), were measured in 42 diabetic patients with abnormalities of LDL particle size, HDL2 percentage and/or Lp(a) levels before and after niacin treatment. LDL particle size and HDL2 were measured using polyacrylamide gradient gel electrophoreses and Lp(a) was measured by enzyme-linked immunoabsorbance assay (ELISA).
  
  
  RESULTS
  After niacin treatment, LDL peak particle diameter increased from 252 +/- 7 A to 263 +/- 7 (p < 0.0001), small, dense LDLc particle mass decreased from 27 +/- 11 mg/dL to 15 +/- 4 (p < 0.0001), total HDLc increased from 39 +/- 7 mg/dL to 51 +/- 11 (p < 0.0001), HDL2 as the percentage of total HDLc mass increased from 29 +/- 8% to 45 +/- 10 (p < 0.0001) and Lp(a) decreased from 43 +/- 17 mg/dL to 25 +/- 10 (p < 0.0001). Mean haemoglobin A1c level was improved during treatment from 7.6 +/- 1.8% to 6.5 +/- 1.0 (p < 0.0001) using increased oral agent and insulin treatment doses in more than 90% of the patients. A total of 21% of the patients were unable to tolerate niacin owing to reversible side-effects, and 14% were unable to adhere to the niacin dosing regimen of three times daily.
  
  
  CONCLUSIONS
  These data indicate that in diabetic patients, niacin (i) is effective for treating diabetic dyslipidaemias associated with both the atherogenic lipid profile and Lp(a); (ii) must be used with modern and aggressive oral hypoglycaemic agents or insulin treatment; and (iii) is an important drug to treat diabetes dyslipidaemias because of its broad spectrum of effectiveness.
authors.affiliation: Diabetes Research Center, Tustin, CA, USA.
authors.forename: J
authors.initials: J
authors.lastname: Pan
authors.forename: M
authors.initials: M
authors.lastname: Lin
authors.forename: R L
authors.initials: RL
authors.lastname: Kesala
authors.forename: J
authors.initials: J
authors.lastname: Van
authors.forename: M A
authors.initials: MA
authors.lastname: Charles
mesh_terms: D001161:Arteriosclerosis / Q000453:epidemiology; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003920:Diabetes Mellitus / Q000097:blood* / Q000188:drug therapy; D003925:Diabetic Angiopathies / Q000517:prevention & control*; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood*; D009525:Niacin / Q000627:therapeutic use*; D012189:Retrospective Studies; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D008055:Lipids; D017270:Lipoprotein(a); D014280:Triglycerides; D009525:Niacin