Effect of smoking on postprandial hypertriglyceridemia

Smokers have recently been shown to be insulin resistant and to exhibit several characteristics of the insulin resistance syndrome that could increase postprandial triglyceridemia. Postprandial hypertriglyceridemia could increase coronary artery disease (CAD) risk. In this study, we assessed fasting and postprandial triglyceride levels in healthy, normolipidaemic, chronic smokers and a matched group of nonsmoking individuals. Methods and Materials: We evaluated 78 subjects with simple sampling in case-control study. 39 were smoker and 39 nonsmokers. All of them had normal lipid and glycemic profile and had BMI between 19 and 29.9. The subjects didn’t have history of CAD or previously elevated fasting TG>150mg/dl, FBS>100mg/dl, age>60or<30, or alcoholic drinking. Then we give them 60 gm butter and triglyceride level was checked one and six hours postprandial. Between these times the subjects should not eat anything except water and smokers were allowed to smoke. All data analyzed with T-test and for repeated data ANOVA with SPSS software. In our study was shown that TG levels among women and men had no significant difference (P=0.403). There was a significant difference among fasting TG, one hour postprandial and six hours postprandial in both groups(P<0.001). Also the changing rate of lipid from fasting state to one and six hours postprandial, among smokers and nonsmokers was significantly different (P<0.001). We concluded that smoking can change lipid profile in normolipemic subjects; and smokers with normal fasting triglyceride have more elevated levels of postprandial triglyceride in compared to nonsmokers. Postprandial hypertriglyceridemia has been an important factor for cardiovascular disease, then smoking can increase cardiovascular disease risk in this way.