1
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
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
Ld lower than the cumulative doses needed to produce cancer in experimental animals [93-96], and beginning in early adolescence, we pair-fed the rats with either high (60 ) or low (5 ) fat containing diets. The NDEA doses were selected to be far below those needed for carcinogenesis and were based on empirical studies demonstrating absence of acute toxic effects in the rats.Longer durations of NDE
1
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,
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
Ld lower than the cumulative doses needed to produce cancer in experimental animals [93-96], and beginning in early adolescence, we pair-fed the rats with either high (60 ) or low (5 ) fat containing diets. The NDEA doses were selected to be far below those needed for carcinogenesis and were based on empirical studies demonstrating absence of acute toxic effects in the rats.Longer durations of NDE
1
Cer. Clin Cancer Res. 2009;15(17):5308?6. 80. Degterev A, Yuan J. Expansion and evolution of cell death programmes. Nat Rev Mol Cell Biol. 2008;9(5):378?0. 81. Shen HM, Codogno P. Autophagy is a survival force via suppression of necrotic cell death. Exp Cell Res. 2012;318(11):1304?. 82. Munoz-Gamez JA, Rodriguez-Vargas JM, Quiles-Perez R, Aguilar-Quesada R, Martin-Oliva D, de Murcia G, et al. PARP
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Ation with impairments in insulin/IGF signaling mechanisms, and deficits in cholinergic and neuronal cytoskeletal gene and protein expression in brain, whereas chronic HFD feeding alone produces more restrictive deficits in insulin/IGF signaling mechanisms with reduced ChAT expression and increased oxidative stress. The combined exposures caused overlapping structural and molecular abnormalities t

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