Hals 2013 J Diabetes Res: Difference between revisions
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|title=Hals IK, Rokstad AM, Strand BL, Oberholzer J, Grill V (2013) Alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. | |title=Hals IK, Rokstad AM, Strand BL, Oberholzer J, Grill V (2013) Alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. J Diabetes Res 2013: 374925. | ||
|info=[http://dx.doi.org/10.1155/2013/374925/ Open Access] | |||
|authors=Hals IK, Rokstad AM, Strand BL, Oberholzer J, Grill V | |authors=Hals IK, Rokstad AM, Strand BL, Oberholzer J, Grill V | ||
|year=2013 | |year=2013 | ||
|journal= | |journal=J Diabetes Res | ||
|abstract=Islet transplantation in diabetes is hampered by the need of life-long immunosuppression. Encapsulation provides partial immunoprotection but could possibly limit oxygen supply, a factor that may enhance hypoxia-induced beta cell death in the early post-transplantation period. Here we tested susceptibility of alginate microencapsulated human islets to experimental hypoxia (0.1-0.3 % O2 for 8 h, followed by re-oxygenation) on viability and functional parameters. Hypoxia reduced viability as measured by MTT by 33.8 ยฑ 3.5 % in encapsulated and 42.9 ยฑ 5.2 % in non-encapsulated islets (p < 0.2). Non-encapsulated islets released 37.7% (median) more HMGB1 compared to encapsulated islets after hypoxic culture conditions (p < 0.001). Glucose-induced insulin release was marginally affected by hypoxia. Basal oxygen consumption was equally reduced in encapsulated and non-encapsulated islets, by 22.0 ยฑ 6.1 % vs. 24.8 ยฑ 5.7 %. Among 27 tested cytokines/chemokines, hypoxia increased the secretion of IL-6 and IL-8/CXCL8 in both groups of islets whereas an increase of MCP-1/CCL2 was seen only with non-encapsulated islets. Conclusion: alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. This is a positive finding in relation to potential use of encapsulation for islet transplantation. | |abstract=Islet transplantation in diabetes is hampered by the need of life-long immunosuppression. Encapsulation provides partial immunoprotection but could possibly limit oxygen supply, a factor that may enhance hypoxia-induced beta cell death in the early post-transplantation period. Here we tested susceptibility of alginate microencapsulated human islets to experimental hypoxia (0.1-0.3 % O2 for 8 h, followed by re-oxygenation) on viability and functional parameters. Hypoxia reduced viability as measured by MTT by 33.8 ยฑ 3.5 % in encapsulated and 42.9 ยฑ 5.2 % in non-encapsulated islets (p < 0.2). Non-encapsulated islets released 37.7% (median) more HMGB1 compared to encapsulated islets after hypoxic culture conditions (p < 0.001). Glucose-induced insulin release was marginally affected by hypoxia. Basal oxygen consumption was equally reduced in encapsulated and non-encapsulated islets, by 22.0 ยฑ 6.1 % vs. 24.8 ยฑ 5.7 %. Among 27 tested cytokines/chemokines, hypoxia increased the secretion of IL-6 and IL-8/CXCL8 in both groups of islets whereas an increase of MCP-1/CCL2 was seen only with non-encapsulated islets. Conclusion: alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. This is a positive finding in relation to potential use of encapsulation for islet transplantation. | ||
|keywords=Human islets, microencapsulation, hypoxia, viability, oxygen consumption, insulin release, cytokine/chemokine secretion | |keywords=Human islets, microencapsulation, hypoxia, viability, oxygen consumption, insulin release, cytokine/chemokine secretion | ||
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{{Labeling | {{Labeling | ||
|area=Respiration | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels [epub ahead of print] | |additional=Labels [epub ahead of print] | ||
}} | }} |
Revision as of 11:56, 12 December 2013
Hals IK, Rokstad AM, Strand BL, Oberholzer J, Grill V (2013) Alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. J Diabetes Res 2013: 374925. |
ยป Open Access
Hals IK, Rokstad AM, Strand BL, Oberholzer J, Grill V (2013) J Diabetes Res
Abstract: Islet transplantation in diabetes is hampered by the need of life-long immunosuppression. Encapsulation provides partial immunoprotection but could possibly limit oxygen supply, a factor that may enhance hypoxia-induced beta cell death in the early post-transplantation period. Here we tested susceptibility of alginate microencapsulated human islets to experimental hypoxia (0.1-0.3 % O2 for 8 h, followed by re-oxygenation) on viability and functional parameters. Hypoxia reduced viability as measured by MTT by 33.8 ยฑ 3.5 % in encapsulated and 42.9 ยฑ 5.2 % in non-encapsulated islets (p < 0.2). Non-encapsulated islets released 37.7% (median) more HMGB1 compared to encapsulated islets after hypoxic culture conditions (p < 0.001). Glucose-induced insulin release was marginally affected by hypoxia. Basal oxygen consumption was equally reduced in encapsulated and non-encapsulated islets, by 22.0 ยฑ 6.1 % vs. 24.8 ยฑ 5.7 %. Among 27 tested cytokines/chemokines, hypoxia increased the secretion of IL-6 and IL-8/CXCL8 in both groups of islets whereas an increase of MCP-1/CCL2 was seen only with non-encapsulated islets. Conclusion: alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. This is a positive finding in relation to potential use of encapsulation for islet transplantation. โข Keywords: Human islets, microencapsulation, hypoxia, viability, oxygen consumption, insulin release, cytokine/chemokine secretion
โข O2k-Network Lab: NO Trondheim Grill V
Labels: MiParea: Respiration
HRR: Oxygraph-2k
Labels [epub ahead of print]