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In brain [85-88]; 2) cause cytotoxicity and insulin resistance [83,88]; and 3) are increased in brains with neurodegeneration [85,89-91]. We measured mRNA levels of ceramide synthases (CER), UDP glucose ceramide glycosyltransferase (UGCG), serine palmitoyltransferase (SPTLC), and sphingomyelin phosphodiesterases (SMPD), due to their demonstrated relevance to neurodegeneration [45,83]. HFD feeding
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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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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 m
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P. Chronic HFD feeding aloneTable 3 Effects of High Fat Diet and NDEA Exposure on Biomarkers of Insulin and IGF Resistance in the CerebellummRNA AbPP Tau AChE ChAT Insulin IGF-1 IGF-2 Insulin R IGF-1R IGF-2R IRS-1 IRS-2 IRS-4 LFD+VEH 7.007 ?0.828 12.230 ?1.098 2.829 ?0.178 0.701 ?0.045 0.754 ?0.048 0.957 ?0.119 12.000 ?1.800 17.090 ?1.547 5.031 ?0.525 5.677 ?0.548 5.559 ?0.411 7.701 ?0.509 0.135 ?
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Ould reduce cases of lenses' falling off.Some patients, (7.1 ) made optometric consultations on account of their lost spectacles with consequential visual discomfort. In a population-based study of spectacles use in southern India, as many as 19.6 of people using spectacles had lost the pairs and could not afford to buy another pairs [21]. The patients should be counselled on how to take good car
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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 m
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R protein; AbPP-Ab: amyloid-b peptide; AChE: acetylcholinesterase; AD: Alzheimer's disease; CER: Ceramide synthase; ChAT: choline acetyltransferase; ELISA: enzyme-linked immunosorbant assay; GFAP: glial fibrillary acidic protein; GSK-3b: glycogen synthase kinase-3b; H E: hematoxylin and eosin; HFD: high fat diet; HNE: 4-hydroxy-2-nonenal; HRP: horseradish peroxidase; i.p.: intraperitoneal; IGF: In
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R protein; AbPP-Ab: amyloid-b peptide; AChE: acetylcholinesterase; AD: Alzheimer's disease; CER: Ceramide synthase; ChAT: choline acetyltransferase; ELISA: enzyme-linked immunosorbant assay; GFAP: glial fibrillary acidic protein; GSK-3b: glycogen synthase kinase-3b; H E: hematoxylin and eosin; HFD: high fat diet; HNE: 4-hydroxy-2-nonenal; HRP: horseradish peroxidase; i.p.: intraperitoneal; IGF: In