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E formation of DNA and protein adducts [105-107] that can serve as persistent sources of oxidative stress, and cause further DNA damage and protein dysfunction. Recently, we demonstrated a role for ceramidemediated neurodegeneration in a model of diet-induced obesity with T2DM [45], and showed that in vitro ceramide exposure causes neurodegeneration with impairments in neuronal viability, energy
N E, Longato L, Jiao P, Mark P, Wands JR, Xu H, de la Monte SM: Hepatic Ceramide May Mediate Brain Insulin Resistance and Neurodegeneration in Type 2 Diabetes and Nonalcoholic Steatohepatitis. J Alzheimers Dis 2009, 16(4):715-729. 46. Moroz N, Tong M, Longato L, Xu H, de la Monte SM: Limited Alzheimertype neurodegeneration in experimental obesity and type 2 diabetes mellitus. J Alzheimers Dis 200
S. Nutr Rev 2007, 65(12 Pt 2):S152-156. 2. Launer LJ: Next steps in Alzheimer's disease research: interaction between epidemiology and basic science. Curr Alzheimer Res 2007, 4(2):141-143. 3. Wang XP, Ding HL: Alzheimer's disease: epidemiology, genetics, and beyond. Neurosci Bull 2008, 24(2):105-109. 4. de la Monte SM, Neusner A, Chu J, Lawton M: Epidemilogical Trends Strongly Suggest Exposures a
D that volatile solvents such as benzene, a main constituent of gasoline fuel, seems to interact with the synthesis and catabolism of catecholamines and serotonin in the brain, which might explain the neurotoxic effects of these solvents [53]. In this regard, deficiencies of serotonin or other monoamine neurotransmitters such as dopamine and norepinephrine are linked with depression [54,55]. In r
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 addit
N E, Longato L, Jiao P, Mark P, Wands JR, Xu H, de la Monte SM: Hepatic Ceramide May Mediate Brain Insulin Resistance and Neurodegeneration in Type 2 Diabetes and Nonalcoholic Steatohepatitis. J Alzheimers Dis 2009, 16(4):715-729. 46. Moroz N, Tong M, Longato L, Xu H, de la Monte SM: Limited Alzheimertype neurodegeneration in experimental obesity and type 2 diabetes mellitus. J Alzheimers Dis 200
Software (GraphPad Software, Inc., San Diego, CA). Software generated significant P-values are shown in the graphs or included in the tables.ResultsEffects of NDEA and HFD on Serum Biomarkers of T2DM (Table 2)Tissue homogenates were prepared in radioimmunoprecipitation assay buffer containing protease and phosphatase inhibitors, as previously described [46]. Direct ELISAs were performed in 96-wel
Enesis. J Neurochem 2002, 82(4):809-818. 113. Mattson MP, Barger SW, Furukawa K, Bruce AJ, Wyss-Coray T, Mark RJ, Mucke L: Cellular signaling roles of TGF beta, TNF alpha and beta APP in brain injury responses and Alzheimer's disease. Brain Res Brain Res Rev 1997, 23(1-2):47-61. 114. Gottfries CG, Karlsson I, Svennerholm L: Membrane components separate early-onset Alzheimer's disease from senile
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 ca
Cells of the rat pancreas. Physiol Res 2001, 50(6):537-546. Doi K: [Studies on the mechanism of the diabetogenic activity of streptozotocin and on the ability of compounds to block the diabetogenic activity of streptozotocin (author's transl)]. Nippon Naibunpi Gakkai Zasshi 1975, 51(3):129-147. Iwai S, Murai T, Makino S, Min W, Morimura K, Mori S, Hagihara A, Seki S, Fukushima S: High sensitivity
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,
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
S. Nutr Rev 2007, 65(12 Pt 2):S152-156. 2. Launer LJ: Next steps in Alzheimer's disease research: interaction between epidemiology and basic science. Curr Alzheimer Res 2007, 4(2):141-143. 3. Wang XP, Ding HL: Alzheimer's disease: epidemiology, genetics, and beyond. Neurosci Bull 2008, 24(2):105-109. 4. de la Monte SM, Neusner A, Chu J, Lawton M: Epidemilogical Trends Strongly Suggest Exposures a
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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