PPARy agonist improves neuronal insulin receptor function in hippocampus and brain mitochondria function in XXXX with insulin resistance induced by long term high-fat diets.

@entity1 @entity308 @entity2308 @entity6 @entity75 @entity35 @entity6170 @entity528 @entity2383
We previously demonstrated that a high-fat diet (HFD) consumption can cause not only peripheral insulin resistance, but also neuronal insulin resistance. Moreover, the consumption of an HFD has been shown to cause @entity2383 in both the skeletal muscle and liver. @entity6170 , a peroxizome proliferator-activated receptor-y ligand, is a drug used to treat @entity6 . Recent studies suggested that @entity6170 can improve learning and memory in both @entity1 and animal models. However, the effects of @entity6170 on neuronal insulin resistance and brain mitochondria after the HFD consumption have not yet been investigated. Therefore, we tested the hypothesis that @entity6170 improves neuronal insulin resistance caused by a HFD via attenuating the dysfunction of @entity528 . @entity6170 (5 mg/kg    d) was given for 14 d to @entity35 that were fed with either a HFD or normal diet for 12 wk. After the 14(th) week, all animals were euthanized, and their brains were removed and examined for insulin-induced long-term @entity308 , neuronal insulin signaling, and brain mitochondrial function. We found that @entity6170 significantly improved peripheral insulin resistance and insulin-induced long-term @entity308 and increased neuronal @entity2308 -ser phosphorylation in response to insulin. Furthermore, @entity6170 prevented brain mitochondrial conformational changes and attenuated brain mitochondrial swelling, brain mitochondrial membrane potential changes, and brain mitochondrial ROS production. Our data suggest that neuronal insulin resistance and the @entity75 caused by a 12-wk HFD consumption can be reversed by @entity6170 .
