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Could serve as biomarkers of insulin-resistance mediated neurodegeneration. Finally, the findings suggest that our insulin resistance disease epidemics are linked to sub-mutagenicTong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 13 ofexposures to nitrosamines and related compounds, combined with chronic consumption of high fat content foods, indicating t
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Or NDEA-associated neurodegeneration and insulin/IGF resistance were likely mediated by increased brain ceramide levels. Those studies demonstrated strikingly increased expression of several genes regulating ceramide production via both de novo biosynthesis or sphingomyelin degradation pathways in NDEA-treated rats, irrespective of chronic HFD feeding. Since NDEA is lipid soluble [115,116] and can
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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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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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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
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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
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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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Ingomyelin phosphodiesterase; SPTLC: Serine palmitoyltransferase; STZ: Streptozotocin; T2DM: Type 2 diabetes mellitus; TBS: Tris buffered saline; UGCG: UDP-glucose ceramide glycoysltransferase. Acknowledgements Supported by AA-11431, AA-12908, and K24-AA-16126 from the National Institutes of Health. Author details 1 Department of Pathology (Neuropathology), Rhode Island Hospital, 593 Eddy Street,

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