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Sodium fluorocitrate having protective effect on palmitate-induced beta cell death improves hyperglycemia in diabetic db/db mice

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dc.contributor.authorJung, IR-
dc.contributor.authorChoi, SE-
dc.contributor.authorHong, SA-
dc.contributor.authorHwang, Y-
dc.contributor.authorKang, Y-
dc.description.abstractBeta cell loss and insulin resistance play roles in the pathogenesis of type 2 diabetes. Elevated levels of free fatty acids in plasma might contribute to the loss of beta cells. The objective of this study was to find a chemical that could protect against palmitate-induced beta cell death and investigate whether such chemical could improve hyperglycemia in mouse model of type 2 diabetes. Sodium fluorocitrate (SFC), an aconitase inhibitor, was found to be strongly and specifically protective against palmitate-induced INS-1 beta cell death. However, the protective effect of SFC on palmitate-induced cell death was not likely to be due to its inhibitory activity for aconitase since inhibition or knockdown of aconitase failed to protect against palmitate-induced cell death. Since SFC inhibited the uptake of palmitate into INS-1 cells, reduced metabolism of fatty acids was thought to be involved in SFC's protective effect. Ten weeks of treatment with SFC in db/db diabetic mice reduced glucose level but remarkably increased insulin level in the plasma. SFC improved impairment of glucose-stimulated insulin release and also reduced the loss of beta cells in db/db mice. Conclusively, SFC possessed protective effect against palmitate-induced lipotoxicity and improved hyperglycemia in mouse model of type 2 diabetes.-
dc.titleSodium fluorocitrate having protective effect on palmitate-induced beta cell death improves hyperglycemia in diabetic db/db mice-
dc.contributor.affiliatedAuthor최, 성이-
dc.contributor.affiliatedAuthor강, 엽-
dc.type.localJournal Papers-
dc.citation.titleScientific reports-
dc.identifier.bibliographicCitationScientific reports, 7(1). : 12916-12916, 2017-
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Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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