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Hepatic G6PD enzymatic activity is diminished in G6PD-deficient individuals (93), can be altered in non-deficient individuals by exogenous factors, such as insulin and high fat diets (94, 95), and can be upregulated to meet increased demand in states of physiologic stress

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NO synthase (eNOS) phosphorylation Furthermore, exenatide reversed homocysteine-induced endothelial dysfunction by decreasing sICAM-1 and reactive oxygen species (ROS) levels and upregulating NO production and eNOS phosphorylation which further contributed the improvement of coronary endothelial function in diabetic patients [58]

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