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      Smoking and Type 2 Diabetes Mellitus

      review-article
      Diabetes & Metabolism Journal
      Korean Diabetes Association
      Diabetes complications, Diabetes mellitus, Smoking

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          Abstract

          Cigarette smoking is a well-known risk factor in many diseases, including various kinds of cancer and cardiovascular disease. Many studies have also reported the unfavorable effects of smoking for diabetes mellitus. Smoking increases the risk of developing diabetes, and aggravates the micro- and macro-vascular complications of diabetes mellitus. Smoking is associated with insulin resistance, inflammation and dyslipidemia, but the exact mechanisms through which smoking influences diabetes mellitus are not clear. However, smoking cessation is one of the important targets for diabetes control and the prevention diabetic complications.

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          Most cited references35

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          Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

          It has been hypothesized that the pathogenesis of diseases induced by cigarette smoking involves oxidative damage by free radicals. However, definitive evidence that smoking causes the oxidative modification of target molecules in vivo is lacking. We conducted a study to determine whether the production of F2-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke. We measured the levels of free F2-isoprostanes in plasma, the levels of F2-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F2-isoprostanes in 10 smokers and 10 nonsmokers matched for age and sex. The short-term effects of smoking (three cigarettes smoked over 30 minutes) and the effects of two weeks of abstinence from smoking on levels of F2-isoprostanes in the circulation were also determined in the smokers. Plasma levels of free and esterified F2-isoprostanes were significantly higher in the smokers (242 +/- 147 and 574 +/- 217 pmol per liter, respectively) than in the nonsmokers (103 +/- 19 and 345 +/- 65 pmol per liter; P = 0.02 for free F2-isoprostanes and P = 0.03 for esterified F2-isoprostanes). Smoking had no short-term effects on the circulating levels of F2-isoprostanes. However, the levels of free and esterified F2-isoprostanes fell significantly after two weeks of abstinence from smoking (250 +/- 156 and 624 +/- 214 pmol per liter, respectively, before the cessation of smoking, as compared with 156 +/- 67 and 469 +/- 108 pmol per liter after two weeks' cessation; P = 0.03 for free F2-isoprostanes and P = 0.02 for esterified F2-isoprostanes). The increased levels of F2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.
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            Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: United Kingdom Prospective Diabetes Study (UKPDS: 23)

            To evaluate baseline risk factors for coronary artery disease in patients with type 2 diabetes mellitus. A stepwise selection procedure, adjusting for age and sex, was used in 2693 subjects with complete data to determine which risk factors for coronary artery disease should be included in a Cox proportional hazards model. 3055 white patients (mean age 52) with recently diagnosed type 2 diabetes mellitus and without evidence of disease related to atheroma. Median duration of follow up was 7.9 years. 335 patients developed coronary artery disease within 10 years. Angina with confirmatory abnormal electrocardiogram; non-fatal and fatal myocardial infarction. Coronary artery disease was significantly associated with increased concentrations of low density lipoprotein cholesterol, decreased concentrations of high density lipoprotein cholesterol, and increased triglyceride concentration, haemoglobin A1c, systolic blood pressure, fasting plasma glucose concentration, and a history of smoking. The estimated hazard ratios for the upper third relative to the lower third were 2.26 (95% confidence interval 1.70 to 3.00) for low density lipoprotein cholesterol, 0.55 (0.41 to 0.73) for high density lipoprotein cholesterol, 1.52 (1.15 to 2.01) for haemoglobin A1c, and 1.82 (1.34 to 2.47) for systolic blood pressure. The estimated hazard ratio for smokers was 1.41 (1.06 to 1.88). A quintet of potentially modifiable risk factors for coronary artery disease exists in patients with type 2 diabetes mellitus. These risk factors are increased concentrations of low density lipoprotein cholesterol, decreased concentrations of high density lipoprotein cholesterol, raised blood pressure, hyperglycaemia, and smoking.
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              Cigarette smoking and fat distribution in 21,828 British men and women: a population-based study.

              To examine the relationship between cigarette smoking habits and fat distribution in a population-based cohort of men and women. We analyzed cross-sectional data from 21,828 men and women who were 45 to 79 years of age, residents in Norfolk, United Kingdom, and were recruited between 1993 and 1997. Cigarette smoking habits and other lifestyle factors were assessed using self-reported questionnaires. Anthropometric measures were obtained during a health examination. Waist-hip ratio was highest among current smokers and least among never smokers after adjusting for age, BMI, alcohol intake, total energy intake, physical activity, and education. Higher waist-hip ratio was directly associated with higher smoking pack-years in current and former smokers and inversely with duration since quitting smoking in former smokers. Adjusting for age, BMI, and other covariates, current smokers had higher waist circumference but lower hip circumference compared with former or never smokers. Cigarette smoking habits seem to influence fat distribution patterns. Although smokers have lower mean BMI compared with nonsmokers, they have a more metabolically adverse fat distribution profile, with higher central adiposity. The explanation for this association may help elucidate the mechanisms underlying the adverse health consequences of cigarette smoking and abdominal obesity.
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                Author and article information

                Journal
                Diabetes Metab J
                Diabetes Metab J
                DMJ
                Diabetes & Metabolism Journal
                Korean Diabetes Association
                2233-6079
                2233-6087
                December 2012
                12 December 2012
                : 36
                : 6
                : 399-403
                Affiliations
                Division of Endocrinology and Metabolism, Department of Internal Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea.
                Author notes
                Corresponding author: Sang Ah Chang. Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Paul's Hospital, The Catholic University of Korea College of Medicine, 180 Wangsan-ro, Dongdaemun-gu, Seoul 130-709, Korea. sangah@ 123456catholic.ac.kr
                Article
                10.4093/dmj.2012.36.6.399
                3530709
                23275932
                0caed744-565f-4b9a-8243-568d0a7b696f
                Copyright © 2012 Korean Diabetes Association

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Review
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                Endocrinology & Diabetes
                diabetes complications,diabetes mellitus,smoking
                Endocrinology & Diabetes
                diabetes complications, diabetes mellitus, smoking

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