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Additionally, obesity and IR both contribute to -cell dysfunction and apoptosis, mechanistically explained by glucotoxicity and increased immunogenicity (the accelerator hypothesis) or by -cell exhaustion due to increased metabolic demand (the overload hypothesis) [23]

The limitation of conventional treatment alone is that it relies entirely on the bodys natural healing rate without augmentation

23 NADPH is also needed for dihydrofolate reductase (DHFR) enzyme to catalyze the reduction of dihydrofolate to tetrahydrofolate (THF) in folate metabolism, which is required for de novo biosynthesis of thymidylate, purines, methionine, and some amino acids

Metabolism of collagen in experimental hyperthyroidism and hypothyroidism in the rat

The intertwining of the RTKs c-MET and EGFR may explain acquired or constitutive EGFR resistance