EFFECTS OF CIGARETTE-SMOKING AND ITS CESSATION ON LIPID-METABOLISM AND ENERGY-EXPENDITURE IN HEAVY SMOKERS
EFFECTS OF CIGARETTE-SMOKING AND ITS CESSATION ON LIPID-METABOLISM AND ENERGY-EXPENDITURE IN HEAVY SMOKERS
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DOI：
10.1172/jci116955
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发表时间：
1994-01-01
影响因子：
15.9
通讯作者：
FAIX, D
中科院分区：
文献类型：
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作者：
HELLERSTEIN, MK;BENOWITZ, NL;FAIX, D
研究了吸烟（CS）的致热和潜在致动脉粥样硬化效应与戒烟之间的关系。重度吸烟者（n = 7，血清可替宁> 200 ng/ ml，> 20支/d）维持等能量恒定饮食2周，1周有CS和1周无CS。在禁食过夜后，在每个阶段的第7天使用间接量热法进行稳定同位素输注。过夜禁食后的CS使静息能量消耗增加5%（与非CS阶段相比不显著; P = 0.18）。CS使FFA通量增加77%，甘油通量增加82%，血清FFA浓度增加73%（P < 0.02），但对脂肪氧化无显著影响。肝脏FFA的再酯化增加超过3倍（P < 0.03），脂肪细胞再循环增加不显著（P = 0.10）。CS诱导的脂质底物循环仅占观察到的能量消耗变化的15%（估计为11千卡/天）。新生肝脏脂肪生成较低（< 1-2 g/d），不受急性CS或慢性停止的影响。肝葡萄糖的产生不受CS，尽管增加血清甘油和FFA通量。停止CS对基础代谢通量没有反弹效应。总之，CS对血脂的致动脉粥样硬化作用的代谢机制（FFA的肝脏再酯化作用增加）已被证实。FFA进入的增加解释了CS诱导的血清PFA浓度的增加。在重度吸烟者中，CS的产热效应很小或不存在，而潜在的致动脉粥样硬化效应得以维持，停止CS不会诱导反弹性脂肪生成环境，该环境特别有利于在不增加食物摄入的情况下增加体脂。
The relationship between thermogenic and potentially atherogenic effects of cigarette smoking (CS) and its cessation was investigated. Heavy smokers (n = 7, serum cotinine > 200 ng/ ml, > 20 cigarettes/d) were maintained on isoenergetic, constant diets for 2 wk, 1 wk with and 1 wk without CS. Stable isotope infusions with indirect calorimetry were performed on day 7 of each phase, after an overnight fast. CS after overnight abstention increased resting energy expenditure by 5% (not significant vs. non-CS phase; P = 0.18). CS increased the flux of FFA by 77%, flux of glycerol by 82%, and serum FFA concentrations by 73% (P < 0.02 for each), but did not significantly affect fat oxidation. Hepatic reesterification of FFA increased more than threefold (P < 0.03) and adipocyte recycling increased nonsignificantly (P = 0.10). CS-induced lipid substrate cycles represented only 15% (estimated 11 kcal/d) of observed changes in energy expenditure. De novo hepatic lipogenesis was low(< 1-2 g/d)and unaffected by either acute CS or its chronic cessation. Hepatic glucose production was not affected by CS, despite increased serum glycerol and FFA fluxes. Cessation of CS caused no rebound effects on basal metabolic fluxes. In conclusion, a metabolic mechanism for the atherogenic effects of CS on serum lipids (increased hepatic reesterification of FFA) has been documented. Increased entry of FFA accounts for CS-induced increases in serum PFA concentrations. The thermogenic effect of CS is small or absent in heavy smokers while the potentially atherogenic effect is maintained, and cessation of CS does not induce a rebound lipogenic milieu that specifically favors accrual of body fat in the absence of increased food intake.