1
Al microenvironment. Cell Cycle. 2010;9(17):3515?3. 56. Martinez-Outschoorn UE, Balliet RM, Rivadeneira DB, Chiavarina B, Pavlides S, Wang C, et al. Oxidative stress in cancer associated fibroblasts drives tumorstroma co-evolution: A new paradigm for understanding tumor metabolism, the field effect and genomic instability in cancer cells. Cell Cycle. 2010;9(16):3256?6. 57. Chiavarina B, Whitaker-M
1
Lusions: Early limited exposure to nitrosamines exacerbates the adverse effects of later chronic high dietary fat intake in promoting T2DM and neurodegeneration. The mechanism involves increased generation of ceramides and probably other toxic lipids in brain.Background The prevalence rates of Alzheimer's Disease (AD), Parkinson's disease (PD), obesity, type 2 diabetes mellitus (T2DM), and metabol
1
Mor microenvironment and its role in promoting tumor growth. Oncogene. 2008;27(45):5904?2. 52. Zamarron BF, Chen W. Dual roles of immune cells and their factors in cancer development and progression. Int J Biol Sci. 2011;7(5):651?. 53. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646?4. 54. Joven J, Guirro M, Marine-Casado R, Rodriguez-Gallego E, Menendez JA.
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
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
Urs), rats were sacrificed by i.p. injection of pentobarbital (120 mg/kg). Blood and cerebella were harvested immediately. Blood or serum was used to measure glucose, insulin, cholesterol, triglycerides, and free fatty acid levels, as previously described [45,46]. Cerebella were harvested for histopathological, biochemical, and molecular studies. For histopathology, tissue samples were immersion f
1
Gs of: 1) increased risk for developing mild cognitive impairment (MCI), dementia, or AD in individuals with T2DM [7,27] or obesity/dyslipidemic disorders [28]; 2) progressive brain insulin resistance andinsulin deficiency in AD [29-32]; 3) cognitive impairment in experimental animal models of T2DM and/or obesity [33,34]; 4) AD-type neurodegeneration and cognitive impairment in experimentally indu
1
S such as diabetes mellitus [74], chronicTong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 3 ofalcoholism [75], or obesity with metabolic syndrome [45,46]. These systemic diseases share in common with primary central nervous system (CNS) degenerative diseases, impairments in cognition, and deficits in insulin and IGF signaling mechanisms, insulin/IGF res