1
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 ?
1
Ause mitochondrial dysfunction [16], ATP deficiency [25] and apoptosis. The structural similarities between STZ and nitrosamines, including N-nitrosodiethylamine (NDEA) and N-nitrosodimethylamine (NDMA) [26], together with experimental evidence that high doses of STZ cause cancer while lower doses cause diabetes or AD-type neurodegeneration with cognitive impairment [15,16,22] led us to hypothesiz
1
Y effects of NDEA on insulin receptor, IGF2 receptor, and IRS-2 were muted by the chronic HFD feeding. Moreover, the main effect of NDEA, irrespective of HFD feeding, was to reduce tau gene expression, whereas chronic HFD feeding, irrespective of NDEA treatment, significantly inhibited ChAT. The only unique effect of HFD+NDEA treatment was to reduce insulin gene expression in the brain.Effects of
1
Changes characterized by focal loss of Purkinje neurons (Fig. 1-A3). NDEA exposure, with or without chronic HFD feeding, resulted in loss of Purkinje cells (Figs. 1-A2, 1-A4) and variable thinning of the granule cell layer. Immunohistochemical staining demonstrated similar levels and distributions of GFAP immunoreactivity in cells distributed in the granule layer of control (Fig 1-B1) and HFD-fed
1
Y effects of NDEA on insulin receptor, IGF2 receptor, and IRS-2 were muted by the chronic HFD feeding. Moreover, the main effect of NDEA, irrespective of HFD feeding, was to reduce tau gene expression, whereas chronic HFD feeding, irrespective of NDEA treatment, significantly inhibited ChAT. The only unique effect of HFD+NDEA treatment was to reduce insulin gene expression in the brain.Effects of
1
Ther hand, recent studies showed that HFD feeding causes obesity, T2DM, and cognitive impairment, but is not sufficient to cause AD [45,46]. Therefore, it's likely that chronic HFD feeding which results in peripheral insulin resistance may provide a second-hit, and that combined with low-dose nitrosamine or other environmental exposures, it may increase the severity of neurodegeneration. In the pr
1
Ds, and cholesterol levels compared with LFD+VEH and LFD +NDEA treated groups. In addition, the serum free fatty acid level was significantly lower in the LFD+NDEA compared with LFD+VEH treated rats, whereas the triglyceride and cholesterol levels were similar in the two groups. Therefore, hyperglycemia, hyper-insulinemia, and hyper-leptinemia were features of chronic HFD feeding, and worsened by
1
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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