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Increase in Circulating Products of Lipid Peroxidation in Smokers With IDDM

  1. Giacomo Zoppini, MD,
  2. Giovanni Targher, MD,
  3. Tiziano Monauni, MD,
  4. Giovanni Faccini, MD,
  5. Elena Pasqualini, PHD,
  6. Carlo Martinelli, MD,
  7. Maria L Zenari, PHD and
  8. Michele Muggeo, MD
  1. Division of Endocrinology and Metabolic Diseases, University of Verona Verona, Italy
  2. Institute of Clinical Chemistry, University of Verona Verona, Italy
  1. Address correspondence and reprint requests to Giacomo Zoppini, MD, Divisione di Endocrinologia e Malattie del Mctabolismo, Ospedale Civile Maggiore, Piazzale Stefani, 1, 1–37126 Verona, Italy.

Abstract

OBJECTIVE To measure plasma malondialdehyde (MDA) concentration, a product of lipid peroxidation, both in IDDM patients and in healthy control subjects and to examine whether smoking has a negative impact on the plasma MDA levels in diabetic patients.

RESEARCH DESIGN AND METHODS Plasma total MDA concentration (as a thiobarbituric acid adduct by high-performance liquid chromatography) was measured in 56 young IDDM patients and in a group of 32 age-, sex-, BMI-, and smoking habit-matched healthy subjects.

RESULTS Plasma MDA concentration in IDDM patients was significantly higher than that in healthy control subjects (mean ± SE: 0.95 ± 0.03 vs. 0.54 ± 0.03 μmol/l; P < 0.0001). After stratification by smoking status, it was seen that diabetic smokers had values of age, BMI, serum lipids, blood pressure, metabolic control, and diabetes duration and its chronic complications superimposable on those of their nonsmoking counterparts. Nevertheless, plasma MDA concentration was significantly higher in IDDM patients who smoked than in IDDM patients who didn't smoke (1.03 ± 0.4 vs. 0.87 ± 0.03 μmol/l; P = 0.002), without any sex difference with regard to MDA levels.

CONCLUSIONS These data show an increase in circulating products of lipid peroxidation in young diabetic smokers, thus further supporting the clinical importance of discouraging the initiation of smoking as well as promoting its cessation in people with IDDM.

  • Received December 14, 1995.
  • Revision received June 13, 1996.
  • Accepted June 13, 1996.
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