Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers

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Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers. / Li, Ping; Nielsen, Hanne Mørck; Müllertz, Anette.

In: Journal of Pharmaceutical Sciences, Vol. 105, No. 9, 09.2016, p. 2743-51.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Li, P, Nielsen, HM & Müllertz, A 2016, 'Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers', Journal of Pharmaceutical Sciences, vol. 105, no. 9, pp. 2743-51. https://doi.org/10.1016/j.xphs.2016.01.006

APA

Li, P., Nielsen, H. M., & Müllertz, A. (2016). Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers. Journal of Pharmaceutical Sciences, 105(9), 2743-51. https://doi.org/10.1016/j.xphs.2016.01.006

Vancouver

Li P, Nielsen HM, Müllertz A. Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers. Journal of Pharmaceutical Sciences. 2016 Sep;105(9):2743-51. https://doi.org/10.1016/j.xphs.2016.01.006

Author

Li, Ping ; Nielsen, Hanne Mørck ; Müllertz, Anette. / Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers. In: Journal of Pharmaceutical Sciences. 2016 ; Vol. 105, No. 9. pp. 2743-51.

Bibtex

@article{0b57de9dd1f24220a6d2364f3dbb2314,
title = "Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers",
abstract = "Self-(nano)-emulsifying drug delivery systems (SNEDDSs) used to deliver peptides and proteins across biological barriers, such as the small intestinal membrane, represents an increasingly interesting field in nanomedicine. Hence, the present study was designed to evaluate the impact of SNEDDS on the transport and uptake mechanisms of insulin across the intestinal membrane. For this purpose, 3 SNEDDS were prepared, and Caco-2 cell monolayers were used to study transport and uptake. The prepared SNEDDSs were all in the range of 35-50 nm and had a negative zeta potential (between -8 and -25 mV). The entrapment of insulin on dispersion in the experimental media ranged from 40{\%} to 78{\%} for all SNEDDSs. Fluorescent microscopy studies indicated that fluorescein isothiocyanate-labeled insulin when administered in solution, as well as when loaded into MCT1 or MCT2 SNEDDS, localized within the intercellular space of the Caco-2 cell monolayer, indicating transport by paracellular diffusion. In contrast, the fluorescein isothiocyanate-labeled insulin in LCT SNEDDS was taken up by the cells. In conclusion, the present study demonstrated that MCT1 and MCT2 SNEDDS, but not LCT SNEDDS increased the transepithelial permeability of insulin, via the paracellular route.",
keywords = "Journal Article",
author = "Ping Li and Nielsen, {Hanne M{\o}rck} and Anette M{\"u}llertz",
note = "Copyright {\circledC} 2016. Published by Elsevier Inc.",
year = "2016",
month = "9",
doi = "10.1016/j.xphs.2016.01.006",
language = "English",
volume = "105",
pages = "2743--51",
journal = "Journal of Pharmaceutical Sciences",
issn = "0022-3549",
publisher = "Elsevier",
number = "9",

}

RIS

TY - JOUR

T1 - Impact of lipid-based drug delivery systems on the transport and uptake of insulin across Caco-2 Cell monolayers

AU - Li, Ping

AU - Nielsen, Hanne Mørck

AU - Müllertz, Anette

N1 - Copyright © 2016. Published by Elsevier Inc.

PY - 2016/9

Y1 - 2016/9

N2 - Self-(nano)-emulsifying drug delivery systems (SNEDDSs) used to deliver peptides and proteins across biological barriers, such as the small intestinal membrane, represents an increasingly interesting field in nanomedicine. Hence, the present study was designed to evaluate the impact of SNEDDS on the transport and uptake mechanisms of insulin across the intestinal membrane. For this purpose, 3 SNEDDS were prepared, and Caco-2 cell monolayers were used to study transport and uptake. The prepared SNEDDSs were all in the range of 35-50 nm and had a negative zeta potential (between -8 and -25 mV). The entrapment of insulin on dispersion in the experimental media ranged from 40% to 78% for all SNEDDSs. Fluorescent microscopy studies indicated that fluorescein isothiocyanate-labeled insulin when administered in solution, as well as when loaded into MCT1 or MCT2 SNEDDS, localized within the intercellular space of the Caco-2 cell monolayer, indicating transport by paracellular diffusion. In contrast, the fluorescein isothiocyanate-labeled insulin in LCT SNEDDS was taken up by the cells. In conclusion, the present study demonstrated that MCT1 and MCT2 SNEDDS, but not LCT SNEDDS increased the transepithelial permeability of insulin, via the paracellular route.

AB - Self-(nano)-emulsifying drug delivery systems (SNEDDSs) used to deliver peptides and proteins across biological barriers, such as the small intestinal membrane, represents an increasingly interesting field in nanomedicine. Hence, the present study was designed to evaluate the impact of SNEDDS on the transport and uptake mechanisms of insulin across the intestinal membrane. For this purpose, 3 SNEDDS were prepared, and Caco-2 cell monolayers were used to study transport and uptake. The prepared SNEDDSs were all in the range of 35-50 nm and had a negative zeta potential (between -8 and -25 mV). The entrapment of insulin on dispersion in the experimental media ranged from 40% to 78% for all SNEDDSs. Fluorescent microscopy studies indicated that fluorescein isothiocyanate-labeled insulin when administered in solution, as well as when loaded into MCT1 or MCT2 SNEDDS, localized within the intercellular space of the Caco-2 cell monolayer, indicating transport by paracellular diffusion. In contrast, the fluorescein isothiocyanate-labeled insulin in LCT SNEDDS was taken up by the cells. In conclusion, the present study demonstrated that MCT1 and MCT2 SNEDDS, but not LCT SNEDDS increased the transepithelial permeability of insulin, via the paracellular route.

KW - Journal Article

U2 - 10.1016/j.xphs.2016.01.006

DO - 10.1016/j.xphs.2016.01.006

M3 - Journal article

C2 - 26921121

VL - 105

SP - 2743

EP - 2751

JO - Journal of Pharmaceutical Sciences

JF - Journal of Pharmaceutical Sciences

SN - 0022-3549

IS - 9

ER -

ID: 169133143