Abstract

BackgroundThe popularity of electronic cigarettes (E-cigarettes) has risen considerably. Several studies have suggested that nicotine may affect insulin resistance, however, the impact of E-cigarette exposure on insulin resistance, an early measure of cardiometabolic risk, is not known.Methods and resultsUsing experimental animals and human data obtained from 3,989 participants of the United States National Health and Nutrition Examination Survey (NHANES), respectively, we assessed the association between E-cigarette and conventional cigarette exposures and insulin resistance, as modelled using the homeostatic model assessment of insulin resistance (HOMA-IR) and glucose tolerance tests (GTT). C57BL6/J mice (on standard chow diet) exposed to E-cigarette aerosol or mainstream cigarette smoke (MCS) for 12 weeks showed HOMA-IR and GTT levels comparable with filtered air-exposed controls. In the NHANES cohort, there was no significant association between defined tobacco product use categories (non-users; sole E-cigarette users; cigarette smokers and dual users) and insulin resistance. Compared with non-users of e-cigarettes/conventional cigarettes, sole E-cigarette users showed no significant difference in HOMA-IR or GTT levels following adjustment for age, sex, race, physical activity, alcohol use and BMI.ConclusionE-cigarettes do not appear to be linked with insulin resistance. Our findings may inform future studies assessing potential cardiometabolic harms associated with E-cigarette use.

Highlights

  • E-cigarettes are battery-powered devices that deliver a nicotine-containing aerosol by heating a liquid containing a solvent, flavorings, and nicotine.[1,2] These novel electronic nicotine delivery systems (ENDS) were originally proposed to be safer alternatives to conventional cigarettes, with potential utility as quit devices

  • Using experimental animals and human data obtained from 3,989 participants of the United States National Health and Nutrition Examination Survey (NHANES), respectively, we assessed the association between E-cigarette and conventional cigarette exposures and insulin resistance, as modelled using the homeostatic model assessment of insulin resistance (HOMA-IR) and glucose tolerance tests (GTT)

  • Cotinine (Fig 1B) and 3-hydroxy cotinine (3HC) (Fig 1C) levels in E-cigarette-exposed mice were comparable with corresponding cotinine and 3HC levels in the urine of mainstream cigarette smoke (MCS)-exposed mice

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Summary

Introduction

E-cigarettes are battery-powered devices that deliver a nicotine-containing aerosol by heating a liquid containing a solvent (vegetable glycerin, propylene glycol, or a mixture of these), flavorings, and nicotine.[1,2] These novel electronic nicotine delivery systems (ENDS) were originally proposed to be safer alternatives to conventional cigarettes, with potential utility as quit devices. Owing to these suggestions of relative safety, aggressive marketing, and less regulation compared to conventional cigarettes,[3] there has been a steady increase in the popularity of these products in both conventional cigarette smokers and non-smokers. Several studies have suggested that nicotine may affect insulin resistance, the impact of Ecigarette exposure on insulin resistance, an early measure of cardiometabolic risk, is not known.

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