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Cited by 155Smoking Behavior and CessationAdipose Tissue and MetabolismDiabetes, Cardiovascular Risks, and Lipoproteins

The DOI matches its Crossref record; 56 of the 57 references it cites were found in a registry or an index; none of the 74 sources its claims cite is checked for support yet.

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

Open access
Hellerstein, M K, Benowitz, N L, Neese, R A, Schwartz, J M, Hoh, R, Jacob, P, Hsieh, J, Faix, D·1994·Journal of Clinical Investigation
DOI 10.1172/jci116955PMC PMC293761
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Abstract

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.

Overview

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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.

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Integrity signals

Registry

Crossref · 10.1172/jci116955

Cites

56 of 56 references verified0 citation errors · 0 not checkable

Statistics

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Verification

Claims the paper makes

0 Valid · 0 Not valid · 39 Not checked · 103 Own results and interpretations

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  • Probably not a substantial claim. 19

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Citations

Cites

Show all 57 references

Research works printed but not linked: 2

  1. E. S. Katkin and S. B. Manuck, editors. Jai Press Inc., Greenwich, Cc. 97-129.
  2. Hellerstein, M. K., R. A. Neese, and J.-M. Schwarz. 1993. Measurement of absolute rates of hepatic de novo lipogenesis and re-esterification of free fatty acids in humans. Am. J. Physiol. In press.

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Metadata

Authors
Hellerstein, M. K., Benowitz, N. L., Neese, R. A., Schwartz, J. M., Hoh, R., Jacob, P., Hsieh, J., & Faix, D.
Affiliations
San Francisco General Hospital (US)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1994-01-01
Volume
93
Issue
1
Pages
265-272
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci116955
PMC
PMC293761
OpenAlex
W2113048216
Semantic Scholar
bf19d755f26608e0b1c7f1b52d3d661afabf17ff
Cited by
155
References
57
Citations by year
2026: 3 · 2025: 4 · 2024: 1 · 2023: 7 · 2022: 7 · 2021: 4 · 2020: 5 · 2019: 6 · 2018: 3 · 2017: 8 · 2016: 3 · 2015: 5 · 2014: 5 · 2013: 5 · 2012: 7
FWCI
12.45
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion, cc-by-nc-sa)
Funders
  • Deutsches Krebsforschungszentrum
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
  • National Institutes of Health (RR-00083)
  • National Institute on Drug Abuse (DA-2277)
  • National Center for Research Resources (M01RR000083, RR 00083)
Topics
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
cigarette smoking, smoking cessation, lipid metabolism, energy expenditure, fatty acid oxidation, hepatic lipogenesis, hepatic glucose production, serum lipids, atherogenic effects, thermogenesis, heavy smokers
MeSH terms
Calorimetry, Cotinine, Energy Metabolism, Fatty Acids, Nonesterified, Glucose, Glycerol, Humans, Liver, Models, Biological, Smoking, Biomarkers, Smoking Cessation, Adipocytes

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