Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB107

Poster Communications

Effect of vape carriers propylene glycol and vegetable glycerine on glucose uptake in airway epithelial cells

M. Woodall1, I. Khan1, R. Tarran2, D. L. Baines1

1. Institute for Infection and Immunity, St George's University of London, London, United Kingdom. 2. Marsico Lung Institute/Cystic Fibrosis Reseach Centre, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States.


Electronic nicotine delivery systems (ENDS), more commonly known as e.cigarettes, are used as a tobacco free nicotine delivery system. ENDS utilise a liquid solution which is drawn over a heating element to produce a vapour which is then inhaled giving rise to the term ‘vaping'. The solution normally contains propylene glycol and vegetable glycerine to generate the vapour together with nicotine and flavourings. Evidence has indicated these carrier chemicals may reduce growth and survival of epithelial cells, including those of the airway[1][2]. As glucose uptake is a key metabolic requirement for cell survival and is critical for the normal function of the airway epithelium, we hypothesised that propylene glycol (PG) and propylene glycol mixed with vegetable glycerine (PG:VG) inhibited glucose uptake human airway epithelial cells. H441 or primary bronchial epithelial cells (HBEC) were grown on plastic or cultured on permeable supports at air-liquid interface. PG (0-3%) or PG:VG (55:45, 0-3%) were applied to the medium, directly to the apical (luminal) surface, or the cells were exposed to vapour for 10 minutes. Glucose uptake across the cell membrane was measured using the Uptake Glo luminescent assay (Promega, UK). Cytotoxicity was measured using an LDH cytotoxicity assay (Peirce, UK). Mannitol (3%) was used as an osmotic control in some experiments. Flourescence recovery after photobleaching (FRAP) was carried out on human embryonic kidney cells transfected with GLUT1-GFP. PG elicited a dose dependent inhibition of glucose uptake in proliferating H441 and HBEC. 3% PG inhibited glucose uptake to a similar level as the glucose transport inhibitor cytochalasin B (35 ± 5% and 32 ± 7% of control p < 0.001, n = 9 respectively). PG did not elicit any changes in LDH release. Treatment of air-liquid interface cultures with PG:VG (3%, 15ml apical) inhibited basolateral but not apical glucose uptake (p<0.01, n=4) in H441 cells and the effect was similar in HBEC when compared to a PBS control. Inhibition was less than that induced by the GLUT transport inhibitor phloretin. No effect of PG:VG on uptake was determined when compared to 3% mannitol. FRAP analysis of GFP linked glucose transporter GLUT1 indicated that both PG:VG and mannitol reduced recovery of fluorescence compared to control. These data indicate that exposure to PG:VG reduces glucose uptake in airway cells via mechanisms that could include osmotic effects and alteration in the turnover of glucose transporters at the membrane.

Where applicable, experiments conform with Society ethical requirements