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Essential phospholipids prevent islet damage induced by proinflammatory cytokines and hypoxic conditions.

Authors :
Shahbazov R
Kanak MA
Takita M
Kunnathodi F
Khan O
Borenstein N
Lawrence MC
Levy MF
Naziruddin B
Source :
Diabetes/metabolism research and reviews [Diabetes Metab Res Rev] 2016 Mar; Vol. 32 (3), pp. 268-77. Date of Electronic Publication: 2015 Oct 28.
Publication Year :
2016

Abstract

Background: The pancreatic islet damage that occurs through an inflammatory response and hypoxia after infusion is a major hurdle in islet transplantation. Because essential phospholipids (EPL) have been shown to exhibit anti-inflammatory properties in liver disease, we analysed their protective effect on islets in inflammatory or hypoxic conditions.<br />Methods: We evaluated the viability of mouse and human islets cultured with cytokines or in hypoxic conditions for 48 h and measured cytokine expression in islets by quantitative polymerase chain reaction. We then employed an in vivo mouse assay, transplanting a marginal dose of human islets treated with or without EPL into the subcapsule of the kidney in diabetic nude mice and determining the cure rate.<br />Results: The viability of mouse and human islets damaged by cytokines was significantly improved by supplementation of EPL in the culture (p = 0.003 and <0.001 for mouse and human islets respectively). EPL significantly inhibited intracellular expression of IL-1β and IL-6 in cytokine-damaged human islets (p < 0.001). The viability of human islets in hypoxic conditions was significantly better when treated with EPL (p < 0.001). In the in vivo mouse assay, the EPL-treated islet group had a higher cure rate than the untreated control, with marginal statistical significance (75 and 17% respectively, p = 0.07).<br />Conclusions: EPL could be a potent agent to protect islets from inflammatory and hypoxic conditions after isolation procedures. Further studies to clarify the effect of EPL in islet transplantation are warranted.<br /> (Copyright © 2015 John Wiley & Sons, Ltd.)

Details

Language :
English
ISSN :
1520-7560
Volume :
32
Issue :
3
Database :
MEDLINE
Journal :
Diabetes/metabolism research and reviews
Publication Type :
Academic Journal
Accession number :
26378630
Full Text :
https://doi.org/10.1002/dmrr.2714