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Long-term exposure of beta cells to saturated fatty acid reduces cellular iron pool, which resulted in unsolved ER stress responses and ultimately beta celldeath.Thus,iron depletion–induced toxicity may be a cause forbeta cellloss during progression oftype 2 diabetes mellitus.My studiessuggestthatattemptstoprotectirondepletionmaybeamaneuverto preventbetacelllossintype2diabetes.However,incautioussupplementation of iron may aggravate the diabetes since iron overload induces insulin resistanceinliverandadiposetissuesoraugmentscytokine-inducedbetacell death.(Dongiovannietal,2013;Gabrielsen etal,2012;Hansen etal,2014;

Tsuchiyaetal,2013).On theotherhands,SFC,aknown aconitaseinhibitor, offers almostcomplete protection againstPA-induced INS-1 celldeath,by reducing PA uptake,rather than by controlling the cellular iron pool,in accordance with the modulation ofiron metabolism-related proteins.Drugs capable ofinhibiting fatty acid uptake have notyetbeen reported.Ifthe molecular mechanism underlying the protective effect of SFC was more clearly elucidated,thiscompound could representan effectivedrug treatment for diabetes,because the inhibition of fatty acid uptake protects against lipotoxicity.

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국문요약

래한다.TCA 회로 중간산물들의 양적 감소 또한 팔미트산 유도 지방 독성에서

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