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P. Chronic HFD feeding aloneTable 3 Effects of High Fat Diet and NDEA Exposure on Biomarkers of Insulin and IGF Resistance in the CerebellummRNA AbPP Tau AChE ChAT Insulin IGF-1 IGF-2 Insulin R IGF-1R IGF-2R IRS-1 IRS-2 IRS-4 LFD+VEH 7.007 ?0.828 12.230 ?1.098 2.829 ?0.178 0.701 ?0.045 0.754 ?0.048 0.957 ?0.119 12.000 ?1.800 17.090 ?1.547 5.031 ?0.525 5.677 ?0.548 5.559 ?0.411 7.701 ?0.509 0.135 ?
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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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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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Xidative stress and neurodegeneration. Cerebellar protein homogenates were used to measure (A) GSK-3b; (B) phospho (p)-GSK-3b; (C) GFAP; (D) GAPDH; (E) HNE; (F) malondialdehyde, MDA; (G) Nitrotyrosine, N-TYR; or (H) b-Actin; by direct binding ELISA. Immunoreactivity was detected with HRP-conjugated secondary antibody and Amplex Red soluble fluorophor. Fluorescence light units (FLU) were measured (
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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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Lusions: Early limited exposure to nitrosamines exacerbates the adverse effects of later chronic high dietary fat intake in promoting T2DM and neurodegeneration. The mechanism involves increased generation of ceramides and probably other toxic lipids in brain.Background The prevalence rates of Alzheimer's Disease (AD), Parkinson's disease (PD), obesity, type 2 diabetes mellitus (T2DM), and metabol
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Ry. Early limited exposure to NDEA had no significant effect on any of the indices measured relative to control. Chronic HFD feeding significantly increased the mean levels of pGSK-3b, GFAP, and N-Tyr relative to all other groups (P