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Therefore, it is plausible that inhibiting FAox when TCA activity is already low and GSSG already high has no further effect, potentially explaining why fibroblasts are refractory to protection by ET

It is known that insulin is involved in neuronal survival, synaptic plasticity, memory, and cognitive function in the central nervous system (CNS), and existing hypotheses suggest that similar to diabetic neuropathy, impaired insulin signalling pathways due to elevated blood glucose and lipids may be the main metabolic mechanism that induces the occurrence of diabetic cognitive dysfunction (6)

During the intercritical phase of GA, persistent oxidative stress leads to significant depletion of glutathione

In: Lieberman HR, Kanarek RB, Prasad C, eds

10.1210/er.2008-0024 82 CornishA

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