Association between smoking and non-alcoholic fatty liver disease: A systematic review and meta-analysis

Rezayat, Arash Akhavan; Moghadam, Malihe; Nour, Mohammad Ghasemi; Shirazinia, Matin; Ghodsi, Hamidreza; Zahmatkesh, Mohammad Reza Rouhbakhsh; Tavakolizadeh, Mitra; Hoseini, Benyamin; Rezayat, Kambiz Akhavan

doi:10.1177/2050312117745223

Cited by 78 publications

(76 citation statements)

References 51 publications

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“…However, we believe that these flaws are balanced by the benefits of this large study, and the ability to generalize these results to the population. As the mechanism of the association between NAFLD and smoking remains controversial, future prospective studies should investigate the underlying mechanisms of this association. In addition, future studies are needed to elucidate the effects of active and passive smoking on NAFLD.…”

Section: Discussionmentioning

confidence: 99%

The interaction of nonalcoholic fatty liver disease and smoking on mortality among adults in the United States

Wijarnpreecha

Scribani

Kim

et al. 2019

Liver International

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Background & Aims Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease in Western countries. Smoking and diabetes mellitus (DM) have been shown to increase mortality; however, whether NAFLD adds to the detrimental effect of smoking in DM and non‐DM patients is unknown. We evaluated the possible interactive effect of NAFLD and smoking on mortality risk in a US population‐based sample. Methods Cross‐sectional data from 11 205 participants in the third National Health and Nutrition Examination Survey were analysed. NAFLD was defined as ultrasonographic hepatic steatosis without evidence of other liver diseases. Proportional hazards regression modelling was used to test for the multiplicative interaction of NAFLD and smoking on overall mortality, controlling for DM. Results 36.5% of the participants had NAFLD of whom 21.1% were current smokers, while among non‐NAFLD subjects, 26.2% reported current smoking. Smoking was associated with a hazard ratio (HR) of 2.23 (95% confidence interval (CI): 1.87‐2.65) among non‐NAFLD subjects, and 2.31 (95% CI: 1.33‐2.92, P < 0.01) among NAFLD patients. In contrast, the HR for NAFLD was 1.01 (95% CI: 0.78‐1.31, P = 0.96) among smokers and 0.98 (95% CI: 0.87‐1.10, P = 0.73) among non‐smokers. There was no evidence of interaction between NAFLD and smoking (HR = 1.01, 95% CI: 0.74‐1.38, P = 0.94) in the combined model. Conclusion We found that smoking increased mortality by two‐fold among the US population. Although the magnitude of the increase in mortality did not differ from that in non‐NAFLD subjects, smoking represents a modifiable determinant of long‐term outcomes in NAFLD patients.

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Section: Discussionmentioning

confidence: 99%

The interaction of nonalcoholic fatty liver disease and smoking on mortality among adults in the United States

Wijarnpreecha

Scribani

Kim

et al. 2019

Liver International

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“…In line with this, in humans, inhalation of nicotine-dense tobacco smoke is associated with a lower body weight, while smoking cessation is accompanied by body weight gain [6,7]. However, inhalation of the broad nAChR-agonist nicotine with smoking is also associated with an increase in cancer risk [8,9], nonalcoholic fatty liver disease [10], and peripheral insulin resistance [11] in humans.…”

Section: Introductionmentioning

confidence: 90%

Pharmacological targeting of α3β4 nicotinic receptors improves peripheral insulin sensitivity in mice with diet-induced obesity

et al. 2020

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Aims/hypothesis Treatment with the α3β4 nicotinic acetylcholine receptor (nAChR) agonist, 1,1-dimethyl-4phenylpiperazinium iodide (DMPP), improves glucose tolerance in diet-induced obese (DIO) mice, but the physiological and molecular mechanisms are unknown. Methods DMPP (10 mg/kg body weight, s.c.) was administered either in a single injection (acute) or daily for up to 14 days (chronic) in DIO wild-type (WT) and Chrnb4 knockout (KO) mice and glucose tolerance, tissue-specific tracer-based glucose metabolism, and insulin signalling were assessed. Results In WT mice, but not in Chrnb4 KO mice, single acute treatment with DMPP induced transient hyperglycaemia, which was accompanied by high plasma adrenaline (epinephrine) levels, upregulated hepatic gluconeogenic genes, and decreased hepatic glycogen content. In contrast to these acute effects, chronic DMPP treatment in WT mice elicited improvements in glucose tolerance already evident after three consecutive days of DMPP treatment. After seven days of DMPP treatment, glucose tolerance was markedly improved, also in comparison with mice that were pair-fed to DMPPtreated mice. The glycaemic benefit of chronic DMPP was absent in Chrnb4 KO mice. Chronic DMPP increased insulinstimulated glucose clearance into brown adipose tissue (+69%), heart (+93%), gastrocnemius muscle (+74%) and quadriceps muscle (+59%), with no effect in white adipose tissues. After chronic DMPP treatment, plasma adrenaline levels did not increase following an injection with DMPP. In glucose-stimulated skeletal muscle, we detected a decreased phosphorylation of the inhibitory Ser640 phosphorylation site on glycogen synthase and a congruent increase in glycogen accumulation following chronic DMPP treatment. Conclusions/interpretation Our data suggest that DMPP acutely induces adrenaline release and hepatic glycogenolysis, while chronic DMPP-mediated activation of β4-containing nAChRs improves peripheral insulin sensitivity independently of changes in body weight via mechanisms that could involve increased non-oxidative glucose disposal into skeletal muscle.

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“…B[a]P was chosen based upon the fact that this carcinogen is a widespread pollutant present in diesel exhaust particles, cigarette smoke and grilled and smoked food, among others [9,10]. Even though a direct link between B[a]P exposure and non-alcoholic fatty liver disease (NAFLD) has been mainly evidenced in rodents [11], different epidemiological studies indicate that high meat consumption, especially grilled meat, as well as cigarette smoking, that is, two major routes of B[a]P exposure, are associated with increased risk of NAFLD [12][13][14][15]. Besides it is important to stress that, for nonsmokers in developed countries, human dietary exposure to B[a]P (0.5-320 ng/day) is generally larger than that by inhalation (0.15-25 ng/day), thus pointing to food ingestion as the main route of exposure to B[a]P for a large part of the general population [16].…”

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confidence: 99%

Mechanisms involved in the death of steatotic WIF-B9 hepatocytes co-exposed to benzo[a]pyrene and ethanol: a possible key role for xenobiotic metabolism and nitric oxide

Tête

Gallais

Imran

et al. 2018

Free Radical Biology and Medicine

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We previously demonstrated that co-exposing pre-steatotic hepatocytes to benzo[a]pyrene (B[a]P), a carcinogenic environmental pollutant, and ethanol, favored cell death. Here, the intracellular mechanisms underlying this toxicity were studied. Steatotic WIF-B9 hepatocytes, obtained by a 48hsupplementation with fatty acids, were then exposed to B[a]P/ethanol (10 nM/5 mM, respectively) for 5 days. Nitric oxide (NO) was demonstrated to be a pivotal player in the cell death caused by the coexposure in steatotic hepatocytes. Indeed, by scavenging NO, CPTIO treatment of co-exposed steatotic cells prevented not only the increase in DNA damage and cell death, but also the decrease in the activity of CYP1, major cytochrome P450s of B[a]P metabolism. This would then lead to an elevation of B[a]P levels, thus possibly suggesting a long-lasting stimulation of the transcription factor AhR. Besides, as NO can react with superoxide anion to produce peroxynitrite, a highly oxidative compound, the use of FeTPPS to inhibit its formation indicated its participation in DNA damage and 1 equal supervision 2 cell death, further highlighting the important role of NO. Finally, a possible key role for AhR was pointed out by using its antagonist, CH-223191. Indeed it prevented the elevation of ADH activity, known to participate to the ethanol production of ROS, notably superoxide anion. The transcription factor, NFB, known to be activated by ROS, was shown to be involved in the increase in iNOS expression. Altogether, these data strongly suggested cooperative mechanistic interactions between B[a]P via AhR and ethanol via ROS production, to favor cell death in the context of prior steatosis.

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Association between smoking and non-alcoholic fatty liver disease: A systematic review and meta-analysis

Cited by 78 publications

References 51 publications

The interaction of nonalcoholic fatty liver disease and smoking on mortality among adults in the United States

The interaction of nonalcoholic fatty liver disease and smoking on mortality among adults in the United States

Pharmacological targeting of α3β4 nicotinic receptors improves peripheral insulin sensitivity in mice with diet-induced obesity

Mechanisms involved in the death of steatotic WIF-B9 hepatocytes co-exposed to benzo[a]pyrene and ethanol: a possible key role for xenobiotic metabolism and nitric oxide

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