PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32442083-7 2020 Plasma BACE1 levels were negatively associated with MoCA, Clock Drawing Test and Logical Memory Test scores, whereas positively associated with Trail Making Test-B time in the MCI group (all p < 0.05), after adjusting fasting blood glucose, glycosylated hemoglobin, and homeostasis model assessment of insulin resistance by C-peptide. Glucose 232-239 beta-secretase 1 Homo sapiens 7-12 33713326-6 2021 High glucose induced the activation of the phosphorylated protein kinase B (pAkt)/GSK-3beta signaling pathway and a significant increase in the expression of beta-site beta APP cleaving enzyme (BACE1), presenilin1 (PS1) and Abeta42. Glucose 5-12 beta-secretase 1 Homo sapiens 194-199 26483636-2 2015 Activity of the aspartic acid protease, beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1), responsible for beta amyloid peptide generation, has recently been demonstrated to modify glucose metabolism. Glucose 199-206 beta-secretase 1 Homo sapiens 101-106 27829662-0 2016 High glucose upregulates BACE1-mediated Abeta production through ROS-dependent HIF-1alpha and LXRalpha/ABCA1-regulated lipid raft reorganization in SK-N-MC cells. Glucose 5-12 beta-secretase 1 Homo sapiens 25-30 26483636-0 2015 BACE1 activity impairs neuronal glucose oxidation: rescue by beta-hydroxybutyrate and lipoic acid. Glucose 32-39 beta-secretase 1 Homo sapiens 0-5 29610518-2 2018 Here we show that the amount of biologically active IR is regulated by the cleavage of its ectodomain, by the beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), in a glucose concentration-dependent manner. Glucose 178-185 beta-secretase 1 Homo sapiens 110-163 29610518-2 2018 Here we show that the amount of biologically active IR is regulated by the cleavage of its ectodomain, by the beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), in a glucose concentration-dependent manner. Glucose 178-185 beta-secretase 1 Homo sapiens 165-170 27829662-2 2016 This study investigated the effect of high glucose on BACE1 expression and amyloidogenesis in vivo, and we present details of the mechanism associated with those effects. Glucose 43-50 beta-secretase 1 Homo sapiens 54-59 26483636-3 2015 We therefore examined, using a human neuroblastoma (SH-SY5Y) cell line, whether increased BACE1 activity is responsible for a reduction in cellular glucose metabolism. Glucose 148-155 beta-secretase 1 Homo sapiens 90-95 26483636-4 2015 Overexpression of active BACE1, but not a protease-dead mutant BACE1, protein in SH-SY5Y cells reduced glucose oxidation and the basal oxygen consumption rate, which was associated with a compensatory increase in glycolysis. Glucose 103-110 beta-secretase 1 Homo sapiens 25-30 26483636-6 2015 This BACE1 activity-dependent deficit in glucose oxidation was alleviated by the presence of beta hydroxybutyrate or alpha-lipoic acid. Glucose 41-48 beta-secretase 1 Homo sapiens 5-10 26483636-7 2015 Consequently our data indicate that raised cellular BACE1 activity drives reduced glucose oxidation in a human neuronal cell line through impairments in the activity of specific tricarboxylic acid cycle enzymes. Glucose 82-89 beta-secretase 1 Homo sapiens 52-57 24752097-4 2014 RESULTS: Compared with the neurons cultured in normal glucose, the neurons exposed to high glucose showed significantly increased Abeta1-42 concentration and BACE-1 mRNA and protein expressions (P<0.05). Glucose 91-98 beta-secretase 1 Homo sapiens 158-164 24752097-6 2014 CONCLUSION: Neurons exposed to high glucose exhibit increased Abeta1-42 levels and BACE-1 mRNA and protein expressions, which can be concentration-dependently decreased by NaHS. Glucose 36-43 beta-secretase 1 Homo sapiens 83-89