title: Effects of gemfibrozil therapy on glucose tolerance, insulin sensitivity and plasma plasminogen activator inhibitor activity in hypertriglyceridaemia.
abstract: BACKGROUND
  Hypertriglyceridaemia (HTG), glucose intolerance, insulin resistance and elevated plasma activity of plasminogen activator inhibitor (PAI)-1 are risk factors for ischaemic heart disease. Because these conditions tend to cluster in the same individuals, the concerted action of gemfibrozil on all these parameters were investigated in a patient group with primary HTG.
  
  
  METHODS
  Gemfibrozil was given as 600 mg tablets twice a day for 12 months to a group of middle-aged non-diabetic men with moderate HTG. Patients served as their own controls, because the treatment period was preceded by a single-blinded 2-month placebo phase. Gradient gel electrophoresis subfractionation of HDL was performed and glucose tolerance was defined according to World Health Organization criteria. The insulin sensitivity was assessed by the insulin-modified minimal model method. Plasma PAI-1 was assayed as activity.
  
  
  RESULTS
  Serum triglyceride concentration was lowered by 49%. Serum high density lipoprotein (HDL) cholesterol concentration was raised by 11% with percentage shift towards the smaller HDL3c subfraction. The low-density lipoprotein cholesterol concentration remained unchanged. The proportion of glucose-intolerant subjects and insulin sensitivity were not altered by gemfibrozil. Plasma PAI-1 activity and fibrinogen levels were unaffected by gemfibrozil. The serum activity of gamma-glutamyltranspeptidase was lowered in all patients.
  
  
  CONCLUSIONS
  Gemfibrozil is safe and effective with regard to its serum triglyceride-lowering potential. However, glucose intolerance, insulin resistance and elevated plasma PAI-1 activity, frequently seen in HTG patients, are not to be expected to be normalized by this drug.
authors.affiliation: King Gustaf V Research Institute, Karolinska Institute, Stockholm, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Asplund-Carlson
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001786:Blood Glucose / Q000187:drug effects; D015248:Gemfibrozil / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D015228:Hypertriglyceridemia / Q000188:drug therapy* / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D007328:Insulin / Q000096:biosynthesis* / Q000097:blood; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000096:biosynthesis* / Q000097:blood; D016896:Treatment Outcome
chemical_list: D001786:Blood Glucose; D000960:Hypolipidemic Agents; D007328:Insulin; D017395:Plasminogen Activator Inhibitor 1; D015248:Gemfibrozil