Rökaeus A, Thor K, Rosell S
Acta Physiol Scand. 1984 Jun;121(2):181-4. doi: 10.1111/j.1748-1716.1984.tb07445.x.
The aim of the present study in man was to investigate the influence of cigarette smoking on basal plasma concentrations of neurotensin-like immunoreactivity (p-NTLI), as well as on fat-induced elevation of p-NTLI levels. On three separate occasions, habitual tobacco smokers either ingested fat (55 ml Intralipid 20%) or smoked three cigarettes, or ingested fat and smoked. The subjects were fasted overnight and told no to smoke during the fasting period. Smoking of one cigarette at one hour intervals (0, 60, and 120 min) did not change the p-NTLI levels (n = 6). Ingestion of fat caused a significant increase (n = 16) and when these two procedures were combined (n = 16), the mean integrated p-NTLI response (nM0-180 min) was 56% larger than the response after fat ingestion alone. The results show that cigarette smoking potentiates the fat-induced elevation of p-NTLI levels, whereas cigarette smoking per se has no effect.
本项人体研究的目的是调查吸烟对基础血浆中神经降压素样免疫反应性(p-NTLI)浓度的影响,以及对脂肪诱导的p-NTLI水平升高的影响。在三个不同的时间段,习惯性吸烟者分别摄入脂肪(55毫升20%英脱利匹特)、吸三支烟或既摄入脂肪又吸烟。受试者隔夜禁食,并被告知在禁食期间不要吸烟。每隔一小时(0、60和120分钟)吸一支烟不会改变p-NTLI水平(n = 6)。摄入脂肪会导致显著升高(n = 16),当这两个过程同时进行时(n = 16),平均整合p-NTLI反应(nM0 - 180分钟)比单独摄入脂肪后的反应大56%。结果表明,吸烟会增强脂肪诱导的p-NTLI水平升高,而吸烟本身没有影响。