Hellerstein M K, Benowitz N L, Neese R A, Schwartz J M, Hoh R, Jacob P, Hsieh J, Faix D
Department of Medicine, San Francisco General Hospital, University of California 94110.
J Clin Invest. 1994 Jan;93(1):265-72. doi: 10.1172/JCI116955.
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 FFA 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.
研究了吸烟（CS）及其戒烟对产热和潜在致动脉粥样硬化作用之间的关系。重度吸烟者（n = 7，血清可替宁>200 ng/ml，每日吸烟>20支）维持等能量、固定饮食2周，其中1周吸烟，1周不吸烟。在每个阶段的第7天，经过一夜禁食后，进行稳定同位素输注并采用间接测热法。过夜 abstention 后吸烟使静息能量消耗增加5%（与不吸烟阶段相比无显著差异；P = 0.18）。吸烟使游离脂肪酸（FFA）通量增加77%，甘油通量增加82%，血清FFA浓度增加73%（每项P < 0.02），但对脂肪氧化无显著影响。肝脏中FFA的再酯化增加了三倍多（P < 0.03），脂肪细胞再循环增加不显著（P = 0.10）。吸烟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 kcal/d）。肝脏从头脂肪生成较低（<1 - 2 g/d），不受急性吸烟或长期戒烟的影响。尽管血清甘油和FFA通量增加，但吸烟对肝脏葡萄糖生成无影响。戒烟对基础代谢通量无反弹效应。总之，已记录到吸烟对血清脂质产生致动脉粥样硬化作用的代谢机制（肝脏中FFA再酯化增加）。FFA进入增加解释了吸烟诱导的血清FFA浓度升高。重度吸烟者中吸烟的产热效应较小或不存在，而潜在的致动脉粥样硬化作用持续存在，并且戒烟不会在没有增加食物摄入的情况下诱导特别有利于身体脂肪积累的脂肪生成环境反弹。 （注：原文中“overnight abstention”表述有误，推测可能是“overnight abstinence”，意为“过夜禁食” ）
