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A role for GLP-1 in regulating glycaemia had been noted in 1986, when this, then newly described ( in vitro , while studies in healthy humans revealed that circulating levels of GLP-1 increased after nutrient intake and confirmed GLP-1 to be an incretin hormone in vivo ( in vitro kinetic studies ( Inhibiting DPP-4 as a Therapy for T2DM In order for this approach to be viable, DPP-4 cleavage would need to be the initial and primary route of metabolism of GLP-1

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RET mutations are detected in all inherited MTC and present in 6% to 10% of apparent sporadic MTC [1]