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The glutamine-glutamate cycle provides neurons with astrocyte-generated glutamate/-aminobutyric acid (GABA) and oxidizes glutamate in astrocytes, and it returns released transmitter glutamate/GABA to neurons after astrocytic uptake. This review deals primarily with the glutamate/GABA generation/oxidation, although it also shows similarity between metabolic rates in cultured astrocytes and intact brain. A key point is identification of the enzyme(s) converting astrocytic α-ketoglutarate to glutamate and vice versa. Most experiments in cultured astrocytes, including those by one of us, suggest that glutamate formation is catalyzed by aspartate aminotransferase (AAT) and its degradation by glutamate dehydrogenase (GDH). Strongly supported by results shown in Table 1 we now propose that both reactions are primarily catalyzed by AAT. This is possible because the formation occurs in the cytosol and the degradation in mitochondria and they are temporally separate. High glutamate/glutamine concentrations abolish the need for glutamate production from α-ketoglutarate and due to metabolic coupling between glutamate synthesis and oxidation these high concentrations render AAT-mediated glutamate oxidation impossible. This necessitates the use of GDH under these conditions, shown by insensitivity of the oxidation to the transamination inhibitor aminooxyacetic acid (AOAA). Experiments using lower glutamate/glutamine concentration show inhibition of glutamate oxidation by AOAA, consistent with the coupled transamination reactions described here. © 2017 by the authors. Licensee MDPI, Basel, Switzerland.


Jia P.,China Medical UniversityLiaoning | Wu N.,The First Affiliated Hospital of China Medical UniversityLiaoning | Zhang X.,China Medical UniversityLiaoning | Jia D.,The First Affiliated Hospital of China Medical UniversityLiaoning
International Journal of Clinical and Experimental Medicine | Year: 2015

Matrix metalloproteinase-1 (MMP-1) has been demonstrated to play an important role in the development and progression of acute coronary syndrome (ACS). Recent studies have shown that MMP-1 -519A/G (rs1144393) polymorphism is associated with the susceptibility to ACS. However, published studies showed inconsistent results. Therefore, a meta-analysis of eligible studies reporting the association between -519A/G polymorphism and ACS was carried out. A systematic search was conducted using PubMed, Web of Science, Cochrane Library, Chinese National Knowledge Infrastructure and Chinese Wan Fang database. Six eligible studies involving 5670 subjects (2868 ACS patients and 2802 healthy controls) were included in this meta-analysis. Overall, this meta-analysis showed a significant association between the rs1144393 polymorphism and ACS (A vs. G: OR = 1.385, 95% CI = 1.019-1.882, P = 0.037; AA vs. AG/GG: OR = 1.547, 95% CI = 1.002-2.389, P = 0.049). Furthermore, subgroup analyses also displayed significant associations between MMP-1 rs1144393 polymorphism and susceptibility to acute myocardial infarction (AA/AG vs. GG: OR = 1.275, 95% CI = 1.016-1.600, P = 0.036) or unstable angina pectoris subjects (A vs. G: OR = 2.128, 95% CI = 1.696-2.670, P < 0.001; AA vs. GG: OR = 2.933, 95% CI = 1.339-6.421, P = 0.007; AA vs. AG/GG: OR = 2.477, 95% CI = 1.457-4.211, P = 0.001). But we found no significant association between the -519A/G polymorphism and ACS either in Asian or Caucasian. In conclusion, our meta-analysis suggests that MMP-1 -519A/G polymorphism was associated with the susceptibility to ACS. However, further large scale case-control studies with rigorous design should be conducted to confirm above conclusions in the future. © 2015, E-Century Publishing Corporation. All rights reserved.


Wu N.,The First Affiliated Hospital of China Medical UniversityLiaoning | Zhang X.,China Medical UniversityLiaoning | Jia P.,China Medical UniversityLiaoning | Jia D.,The First Affiliated Hospital of China Medical UniversityLiaoning
International Journal of Clinical and Experimental Medicine | Year: 2015

A single nucleotide polymorphism (rs4804611) in zinc finger protein 627 (ZNF627) gene has been demonstrated to be associated with the susceptibility to myocardial infarction (MI), but the results are inconsistent. Therefore, a meta-analysis of eligible studies reporting the association between rs4804611 and MI was carried out to enhance the reliability of published results. A systematic literature search was performed using PubMed, Web of Science, Cochrane Library to search English articles concerning the relation between rs4804611 and MI up to January, 2015. Summary odds ratios (OR) and 95% confidence interval (CI) were used to evaluate the risk of MI. The heterogeneity and publication bias of this study were also evaluated. Five eligible studies involving 11639 subjects (6299 patients and 5340 healthy controls) were included in this meta-analysis. Overall, the results indicated that rs4804611 polymorphism was associated with the risk of MI (GG vs. AA/AG: OR = 0.833, 95% CI = 0.704-0.985, P = 0.033). Furthermore, subgroup analyses also showed that rs4804611 polymorphism was associated with the risk of MI in Caucasian (GG vs. AA/AG: OR = 0.839, 95% CI = 0.704-0.999, P = 0.048). In conclusion, our meta-analysis suggests that the rs4804611 polymorphism in ZNF627 gene is associated with the risk of MI. However, further large scale case-control studies with rigorous design should be conducted to confirm the conclusion in the future. © 2015, E-Century Publishing Corporation. All rights reserved.

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