title: The insulin resistance syndrome and postprandial lipid intolerance in smokers.
abstract: BACKGROUND
  The effects of cigarette smoking on insulin resistance, postprandial lipemia following a mixed meal, lipoproteins and other aspects of the insulin resistance syndrome (IRS) were investigated in healthy middle-aged men.
  
  
  METHODS
  36 smoking and 25 age- and body mass index (BMI)-matched non-smoking men participated. They were non-obese (BMI < 27), healthy and without any medication. The smokers had been smoking more than 10 cigarettes per day for more than 20 years; the non-smokers had never been habitual smokers. Body composition and several metabolic and cardiovascular risk factors were studied, including the prevalence of small dense LDL-particles, lipoprotein and hepatic lipase activity and triglyceride levels after a mixed test meal. For determination of degree of insulin sensitivity the euglycemic hyperinsulinemic clamp technique was used.
  
  
  RESULTS
  The smokers had lower HDL-cholesterol and lipoprotein A-I levels but higher fasting triglycerides, as well as an increased proportion of small dense LDL-particles and higher postheparin hepatic lipase activity. They also had higher levels of fibrinogen, plasminogen activator inhibitor 1 (PAI-1) activity and fasting and steady-state C-peptide levels during the clamp. The smokers were insulin resistant and lipid intolerant with an impaired triglyceride clearance after a mixed test meal. This lipid intolerance was not mirrored by fasting hypertriglyceridemia.
  
  
  CONCLUSIONS
  This study, using the euglycemic hyperinsulinemic clamp technique, shows that smokers are both insulin resistant and lipid intolerant. The postprandial lipid intolerance is also seen in individuals with normal fasting triglyceride levels and is related to an increased prevalence of atherogenic small dense LDL. IRS is likely to be an important reason for the increased cardiovascular morbidity in smokers.
authors.affiliation: Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg, Sweden. bjorn.eliasson@medicine.gu.se
authors.forename: B
authors.initials: B
authors.lastname: Eliasson
authors.forename: N
authors.initials: N
authors.lastname: Mero
authors.forename: M R
authors.initials: MR
authors.lastname: Taskinen
authors.forename: U
authors.initials: U
authors.lastname: Smith
mesh_terms: D000328:Adult; D016633:Apolipoprotein A-II / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D005340:Fibrinogen / Q000378:metabolism; D015309:Glucose Clamp Technique; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood*; D008071:Lipoprotein Lipase / Q000097:blood; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D019518:Postprandial Period / Q000502:physiology*; D011863:Radioimmunoassay; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000097:blood / Q000503:physiopathology; D013577:Syndrome; D014527:Uric Acid / Q000097:blood
chemical_list: D016633:Apolipoprotein A-II; D001055:Apolipoproteins B; D001786:Blood Glucose; D002096:C-Peptide; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; D014527:Uric Acid; D005340:Fibrinogen; D008071:Lipoprotein Lipase