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We measured gene expression corresponding to insulin and IGF polypeptides and receptors, and insulin receptor substrates (IRSs) that transmit signals required for growth, survival, energy metabolism, and neuronalELISAs were used to measure sustained effects of NDEA treatment and/or chronic HFD feeding on Tau, phospho-Tau, AbPP, AbPP-Ab, ChAT, and AChE levels in brain tissue. Early limited exposure
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Affected in AD, as well as other neurodegenerative diseases [47,50, 53,56,59,60,65,68,69,71], and cerebellar degeneration causes cognitive impairment [49,57-59,62,63,66,67,72]. Previous studies demonstrated significant structural, functional, and metabolic abnormalities in AD cerebella [57-59,82], including insulin and IGF resistance [30],similar to the findings in more traditional targets of AD,
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N.edu 1 Department of Pathology (Neuropathology), Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903, USAnoted that the striking increases in AD and PD mortality rates followed sharply increased consumption of processed foods, use of preservatives, and demand for nitrogen-containing fertilizers [4]. A common theme resonating from these unnecessary lifestyle trends is that we have inadver
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D (Ex 579 nm/Em 595 nm) in a Spectromax M5, and results were normalized to sample protein content in the wells. Box plots depict mean, range ?S.D. of results (N = 8-10/group). Inter-group comparisons were made using ANOVA with the post-hoc Bonferroni multiple comparisons test of significance. Significant P-values are indicated within the panels.Tong et al. BMC Endocrine Disorders 2010, 10:4 http:/
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N exist inTable 2 High Fat Diet Feeding and NDEA Treatment Cause Type 2 Diabetes MellitusAssay Body Wt (g) Glucose (mg/dL) Insulin (ng/ml) Leptin Adiponectin Triglyceride (mg/ml) Free Fatty Acids (mM/mg prot) Cholesterol (mg/ml) LFD+VEH 265.100 ?14.050 111.5 ?1.66 0.0611 ?0.017 4.649 ?0.789 20864 ?1454 0.399 ?0.028 0.150 ?0.003 0.943 ?0.024 LFD+NDEA 266.600 ?19.970 128.8* ?4.31 0.163* ?0.038 4.775
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F HNE were similar in the HFD+VEH and HFD+NDEA groups, and both were significantly higher than in the LFD+VEH and LFD +NDEA groups (P
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N in ways that could cause insulin/IGF resistance in the brain, their specific effects were not identical. The main effect of NDEA, with or without HFD feeding, was to reduce mRNA levels of insulin receptor, IGF-2 receptor, and IRS-2, which would have impaired signaling at the receptor level, and downstream through IRS-2, one of main docking proteins responsible for transmitting survival, growth,
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Www.biomedcentral.com/1472-6823/10/Page 6 ofthe context of peripheral insulin resistance or T2DM. Similar results have been reported previously, in which the investigators generated models with much higher doses of NDEA [84]. One potential explanation for this paradox is that homeostatic mechanisms may have shifted toward increased storage of lipids/triglycerides in adipose tissue, skeletal muscle

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