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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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Res of AD cerebellar atrophy include, reductions in Purkinje cell population, atrophy of the molecular and granule cell layers [68], increased amyloid deposition and gliosis in the cortex [69]; increased ubiquitin-immunoreactivity in senile plaques and degenerating neurites [70]; extensive abnormalities in dendritic spine density and synaptic structure in vestibulocerebellar, visual, and auditory
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Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
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Ration have soared over the past several decades, suggesting that exposures rather than genetics dictate their etiologies. Our over-arching hypothesis is that shifts in lifestyles and economics have led us to chronically consume excess fat, and get exposed to agents that cause insulin resistance. Consideration given to potential pathogenic agents was focused by the experimental evidence showing th
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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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Ration have soared over the past several decades, suggesting that exposures rather than genetics dictate their etiologies. Our over-arching hypothesis is that shifts in lifestyles and economics have led us to chronically consume excess fat, and get exposed to agents that cause insulin resistance. Consideration given to potential pathogenic agents was focused by the experimental evidence showing th
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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
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R-group comparisons were made using ANOVA with the post-hoc Bonferroni multiple comparisons test of significance. Significant P-values are indicated within the panels.suggesting that early life exposures may contribute to the pathogenesis of AD, perhaps through gene imprinting. Although chronic HFD feeding and limited NDEA exposure increased body weight and caused T2DM/peripheral insulin resistanc