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Clearly, -estradiol is protective against complications arising from impaired extra mitochondrial processing of 16:0.In addition, it was observed that blood glucose levels of female PPAR (-/-) mice recovered relatively quickly to Etomoxir-induced hypoglycemia but that male PPAR (-/-) did not.-Estradiol pretreated male PPAR (-/-) exhibited a similar result as female PPAR (-/-) mice.These data are consistent with the data of [166] in that recovery from insulin-induced hypoglycemia was significantly slower in autistic children versus non-autistic children.This hypoglycemic response is relevant in that glutamate toxicity creates localized hypoglycemia presumably due to increased glucose uptake [156].In addition, -estradiol increases lactate dehydrogenase activity and synthesis [167] as well as lactate export [156], which increases glycolysis flux capacity.-estradiol also increases cytosolic acetyl-CoA utilization by increasing fatty acid synthase and acetyl-CoA carboxylase activity [168], which would irreversibly remove acetyl-CoA from the cytosolic pool and free up cytosolic carnitine, which would enhance mitochondrial processing of 16:0

Mondal S, Choudhury K, Sharma S, Gupta A, Dutta S

doi: 10.1074/jbc.RA118.003180 71 PetkeviciusKVirtueSBidaultGJenkinsBCubukCMorgantiniCet al

Evidence for T-helper 2 shift and association with illness parameters in chronic fatigue syndrome (CFS)