LIPID INTOLERANCE IN SMOKERS

Objectives, Smokers have recently been shown to be insulin resistant a nd to exhibit several characteristics of the insulin resistance syndro me (IRS). In this study, rye assessed fasting and postprandial lipid l evels in healthy, normolipidaemic, chronic smokers and a matched group of non-smoking individuals. Design, A standardized mixed meal (contai ning 3.78 MJ and 51 g of fat) was given in the morning after an overni ght fast, The smokers were either abstinent from tobacco for 48 h or w ere allowed to smoke freely, including being allowed to smoke six ciga rettes during the study. Subjects. Twenty-two middle-aged, healthy mal e subjects, nine habitual smokers and 13 non-smoking control subjects, were recruited to the study, The smokers had all been smoking at leas t 10 cigarettes per day for at least 10 years. Results. The smokers ex hibited a lipid intolerance in that their postprandial increase in tri glyceride levels was more than 50% higher than in the non-smokers grou p. This lipid intolerance could not be discerned in the postabsorptive state because the fasting triglyceride levels were the same in both g roups, whilst the smokers had significantly lower high-density lipopro tein (HDL) cholesterol. The peak postprandial triglyceride level corre lated closely and negatively with fasting HDL cholesterol, indicating an impaired lipolytic removal capacity in smokers. Conclusions, Health y, normotriglyceridaemic smokers exhibit an abnormal postprandial lipi d metabolism consistent with lipid intolerance. It is suggested that p ostprandial hyperlipidaemia is a characteristic trait of the insulin r esistance syndrome and that the defect in lipid removal is related to the low HDL cholesterol in this syndrome, The insulin resistance syndr ome is likely to be an important reason for the increased propensity f or cardiovascular disease in smokers.