期刊
ACTA DIABETOLOGICA
卷 49, 期 3, 页码 167-183出版社
SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s00592-011-0364-z
关键词
L-Glutamic acid; Glutamate toxicity; Monosodium glutamate; Obesity; Diabetes; Pancreatic beta-cells
资金
- University Research Program
- National Institutes of Health [RO1 DK080148]
In the present article, we propose the perspective that abnormal glutamate homeostasis might contribute to diabetes pathogenesis. Previous reports and our recent data indicate that chronically high extracellular glutamate levels exert direct and indirect effects that might participate in the progressive loss of beta-cells occurring in both T1D and T2D. In addition, abnormal glutamate homeostasis may impact all the three accelerators of the accelerator hypothesis and could partially explain the rising frequency of T1D and T2D.
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