Dimethyl amiloride improves glucose homeostasis in mouse models of type 2 diabetes.

American Journal of Physiology. Endocrinology and Metabolism
Subhadra C GunawardanaDavid W Piston

Abstract

Dimethyl amiloride (DMA) enhances insulin secretion in the pancreatic beta-cell. DMA also enhances time-dependent potentiation (TDP) and enables TDP to occur in situations where it is normally absent. As we have demonstrated before, these effects are mediated in part through inhibition of neuronal nitric oxide synthase (nNOS), resulting in increased availability of arginine. Thus both DMA and arginine have the potential to correct the secretory defect in diabetes by enabling or enhancing TDP. In the current study we have demonstrated the ability of these agents to improve blood glucose homeostasis in three mouse models of type 2 diabetes. The pattern of TDP under different conditions indicates that inhibition of NOS is not the only mechanism through which DMA exerts its positive effects. Thus we also have explored another possible mechanism through which DMA enables/enhances TDP, via the activation of mitochondrial alpha-ketoglutarate dehydrogenase.

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Citations

Dec 25, 2010·Proceedings of the National Academy of Sciences of the United States of America·Stanley Y ShawStuart L Schreiber
May 4, 2010·Chemico-biological Interactions·Kehkashan ParveenWaseem A Siddiqui
Oct 9, 2021·The Journal of Clinical Investigation·Matthew R BrownAleksey V Matveyenko

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