IMPACT OF CHRONIC CIGARETTE-SMOKING ON BODY-COMPOSITION AND FUEL METABOLISM

Cigarette smoking has been associated with increased upper body fat de position, as estimated by the waist to hip ratio, which has been shown to be associated with glucose intolerance and dyslipidemia in nonsmok ing subjects. Whether smoking is at the origin of central adiposity an d its related metabolic disturbances is unclear. Moreover, it is contr oversial whether smoking influences fuel metabolism. Therefore, young healthy male volunteers smoking more than 10 cigarettes/day for more t han 5 yr (n = 14) were compared with nonsmokers (n = 13) matched for a ge, sex, body mass index, alcohol consumption, physical activity, as w ell as family history for hyper tension, diabetes, obesity, and corona ry heart disease. After an overnight fast, blood was drawn for chemist ry, body composition was assessed by dual energy x-ray absorptiometry, and fuel metabolism was determined by indirect calorimetry. Nicotine uptake was estimated by 24-h urinary excretion of cotinine. Lean and f at body mass as well as their respective segmental distribution (i.e. arms, trunk, legs, and head), total bone mineral content, resting ener gy expenditure, and fat, carbohydrate, and protein oxidation were simi lar between smokers and nonsmokers. In contrast, 24-h urinary cotinine excretion (72.0 +/- 11.4 vs. 0.8 +/- 0.2 mu mol/L . 24 h; P < 0.001), plasma glucose (4.62 +/- 0.09 vs. 4.25 +/- 0.1 mmol/L; P < 0.01), tot al cholesterol (4.87 +/- 0.15 vs. 4.27 +/- 0.16 mmol/L; P < 0.02), low density lipoprotein cholesterol (3.05 +/- 0.19 v s. 2.43 +/- 0.16 mmo l/L; P < 0.02), and apolipoprotein B concentrations (1.09 +/- 0.11 vs. 0.83 +/- 0.03 mmol/L ; P < 0.031 were all higher in smokers than in n onsmokers. In smokers, 24-h urinary cotinine excretion positively corr elated with the waist to hip ratio (r = 0.58; P = 0.03) and negatively with hip circumference (r = 0.87; P < 0.001). Moreover, 24-h cotinine excretion positively correlated with fat oxidation (r = 0.57; P = 0.0 3), but was independent of the other metabolic parameters studied. The se results suggest that the dyslipidemia and glucose intolerance obser ved in smokers are not related io either central obesity or the amount of nicotine inhaled, but, rather, are due to some other component in cigarette smoke. In contrast, in smokers, fat oxidation increases with increasing nicotine uptake, a fact that might account for the often o bserved weight gain after cessation of smoking, thus suggesting differ ent mechanisms of action of tobacco consumption on cholesterol and glu cose metabolism on one side and fat oxidation on the other.