Effects of cigarette smoking and its cessation on lipid metabolism and energy expenditure in heavy smokers.

TL;DR

In seven heavy smokers on a metabolic ward, acute cigarette smoking increased lipolysis and hepatic FFA reesterification but produced only a small, nonsignificant rise in resting energy expenditure. Smoking cessation did not induce a rebound lipogenic or reduced-fat-oxidation state that would favor body-fat gain in the absence of increased food intake.

Key findings

• Acute smoking after overnight abstinence increased resting energy expenditure by 4.6% (64.4±3.5 to 67.3±3.9 kcal/h), which was not statistically significant versus the non-smoking phase (P = 0.18).
• Acute smoking increased FFA flux by 77%, glycerol flux by 82%, and serum FFA concentrations by 73% (P < 0.02 for each), without significantly affecting fat oxidation.
• Hepatic reesterification of FFA increased more than threefold (0.59±0.48 to 2.03±0.54 µmol/kg per min; P < 0.03), while adipocyte recycling increased nonsignificantly (P = 0.10); lipid substrate cycles accounted for 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 acute smoking or cessation; hepatic glucose production was not affected, and cessation caused no rebound effects on basal metabolic fluxes.

Methods

• Seven heavy smokers (serum cotinine >200 ng/ml, >20 cigarettes/d) completed a 2-wk inpatient metabolic ward study with randomized 1-wk smoking and 1-wk non-smoking phases on a constant, weight-maintaining diet.
• On day 7 of each phase, after an overnight fast, subjects received stable isotope infusions ([1-13C]acetate, [d5]-glycerol, [1,2,3,4-13C]palmitate, and [6,6-d2]-glucose) with indirect calorimetry; they smoked one cigarette every 30 min from 9:00 a.m. to noon in the smoking phase or did not smoke.
• Rates of appearance were calculated by isotope dilution; FFA reesterification was calculated using the Wolfe/Klein method, and fractional de novo lipogenesis was measured by mass isotopomer distribution analysis; comparisons used two-factor repeated measures ANOVA.

Limitations

• The paper states that the 1-wk smoking and non-smoking periods were not long enough for differences in fasting serum lipoproteins to become apparent.
• The paper states that the absolute DNL method may underestimate DNL if tissues oxidize endogenous fat stores that did not traverse the circulation, and that the technique relies on several assumptions.
• Evident from the text: the sample was very small (n = 7) and restricted to heavy smokers, so findings may not generalize to light smokers; withdrawal scores were not measured.