男性吸烟者体重对烟碱引起的生热作用和儿茶酚胺释放的影响(英文)

Effects of body mass on nicotine-induced thermogenesis and catecholamine release in male smokers

本研究的目的是在中年男子中观察禁食情况下吸烟后烟碱对安静时能量消耗 (restingenergyexpendi ture ,REE)和血浆儿茶酚胺浓度的影响 ;并且在正常体重 (BMI≤ 2 5kg/m2 )和超重 (BMI >2 5kg/m2 )吸烟者之间比较吸烟引起的REE和血浆儿茶酚胺的急性反应是否有差别。对 32名禁食的男性吸烟者用间接测热法分别在吸烟前和吸 2支含 0 16mg烟碱 (低烟碱 )或 2支含 1 74mg烟碱 (高烟碱 )香烟 30min后测定REE ,同时测定血浆中烟碱和去甲肾上腺素浓度。正常体重组在吸低烟碱烟后和超重组不论在吸低烟碱烟或高烟碱烟后 ,REE和血浆儿茶酚胺均无明显改变。而在正常体重组中 ,吸高烟碱烟后血浆去甲肾上腺素浓度升高 ,同时REE增加7 2 % ;如果将血浆烟碱水平作为一个共变量进行分析 ,则吸烟后血浆去甲肾上腺素浓度和REE的改变也不明显 ,表明吸烟后的生热效应是因血浆烟碱浓度升高而引起的。体重对烟碱的生热效应能发生影响 ,在超重的吸烟者中烟碱的生热效应减弱。由此推测 ,正常体重的吸烟者在戒烟后 ,由于不再有吸烟引起的耗能生热 。

The aims of this study were: to examine the effects of nicotine on resting energy expenditure (REE) and plasma catecholamine release following ad libitum smoking in fasted, middle aged males; and, to determine if the acute responses in REE and catecholamine release to smoking differ between normal weight (≤25 kg/m 2) and overweight (>25 kg/m 2) smoker groups. REE was measured by indirect calorimetry in 32 fasted male smokers prior to, and 30 minutes after, consuming either two 0 16 mg nicotine (low yield) or two 1 74 mg nicotine (high yield) cigarettes. Plasma nicotine and norepinephrine levels were simultaneously measured. There was no thermic effect of nicotine or catecholamine response after smoking low yield cigarettes in both groups, nor after smoking high yield cigarettes in the overweight group. In contrast, REE increased 7 2%, which was accompanied by an increase in plasma norepinephrine release, after smoking high yield cigarettes in the normal weight group. Controlling plasma nicotine level ablated these increases. In conclusion, body mass interacts with the thermic effect of nicotine and neuroendocrine function in male smokers. Smoking induced increase in the plasma nicotine level accounts for the observed responses, which are blunted in overweight smokers. This finding may have implications for potential weight gain following smoking cessation by normal weight individuals, related to lost smoking induced thermogenesis.