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Sulin receptor substrate gene expression, and reduced expression of tau and choline acetyltransferase (ChAT), which are regulated by insulin and IGF-1. In addition, increased levels of 4-hydroxynonenal and nitrotyrosine were measured in cerebella of HFD ?NDEA treated rats, and overall, NDEA+HFD treatment reduced brain levels of Tau, phospho-GSK-3b (reflecting increased GSK-3b activity), glial fibr
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Urs), rats were sacrificed by i.p. injection of pentobarbital (120 mg/kg). Blood and cerebella were harvested immediately. Blood or serum was used to measure glucose, insulin, cholesterol, triglycerides, and free fatty acid levels, as previously described [45,46]. Cerebella were harvested for histopathological, biochemical, and molecular studies. For histopathology, tissue samples were immersion f
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Urces. Therefore, we entertained the hypothesis that either limited or chronic low-level exposures to nitrosamines account for the observed shifts in morbidity and mortality from insulin resistance diseases. Moreover, given the clear role of high dietary fat intake as a mediator of obesity, T2DM, or cognitive impairment, we proposed that the combined effects of HFD and NDEA exposure may act additi