title: Insulin resistance and arteriosclerosis obliterans in patients with NIDDM.
abstract: OBJECTIVE
  To investigate the risk factors for arteriosclerosis obliterans (ASO) in NIDDM, we measured insulin sensitivity and other risk factors including lipoprotein(a) [Lp(a)] in NIDDM patients with and without ASO.
  
  
  METHODS
  A case-control study in 100 patients with NIDDM, 35 with and 65 without ASO, was performed. Insulin sensitivity was assessed by the short insulin tolerance test's K index (KITT). Duration of diabetes, a history of smoking, prevalence of hypertension, prevalence of coronary artery disease (CAD), serum C-peptide, 24-h urinary C-peptide, serum lipids, and Lp(a) were compared in the two groups.
  
  
  RESULTS
  Age, BMI, HbA1c, and fasting plasma glucose were comparable in the two groups. Patients with ASO were significantly more insulin resistant than patients without ASO (KITT 2.16 +/- 0.16 vs. 3.00 +/- 0.13%/min, P < 0.0001, respectively), had a longer duration of diabetes (10.3 +/- 1.2 vs. 7.5 +/- 0.8 years, P < 0.05), included a greater number of smokers (68.6 vs. 40.0%, P < 0.01), had a higher prevalence of CAD (60.0 vs. 16.9%, P < 0.01), and had a greater percentage of insulin therapy (48.6 vs. 29.2%, P < 0.05). However, urinary and serum C-peptide levels, serum lipids, and Lp(a) levels were comparable in the two groups. Multiple logistic regression analysis indicated that a history of smoking (odds ratio 3.70, P = 0.011), insulin resistance (odds ratio 3.68, P < 0.001), and an elevated Lp(a) level (odds ratio 1.03, P = 0.020) were independently related to ASO. When patients with CAD were removed from the logistic regression analysis, insulin resistance was most strongly related to ASO (odds ratio 20.9, P < 0.001).
  
  
  CONCLUSIONS
  Patients with ASO were characterized by a higher prevalence of CAD, a greater percentage of smokers, a greater percentage of insulin therapy, and a higher insulin resistance than were patients without ASO. Insulin resistance, especially, may be the most powerfully related to ASO. Lp(a) may play a minor role in the development of ASO.
authors.affiliation: Department of Internal Medicine, Sasebo Chuou Hospital, Nagasaki, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Matsumoto
authors.forename: S
authors.initials: S
authors.lastname: Miyake
authors.forename: M
authors.initials: M
authors.lastname: Yano
authors.forename: Y
authors.initials: Y
authors.lastname: Ueki
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaguchi
authors.forename: S
authors.initials: S
authors.lastname: Akazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Tominaga
mesh_terms: D000368:Aged; D001162:Arteriosclerosis Obliterans / Q000209:etiology* / Q000503:physiopathology; D016022:Case-Control Studies; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D012307:Risk Factors
chemical_list: D008055:Lipids; D017270:Lipoprotein(a)