After the release of incriminating evidence of kicking the heart & bone breaking habits of Rosi she is out of the glittering zone for the RECORD sake. Sita!,as we heard of your harmonious gutsy nature we seek your help in mitigating glucotoxicity & increasing insulin sensitivity in our treat to target projects.The knockout game is on!
We don't want any more trials like ACCORD where the punishment of the subjects is done even before the release of judgment for no fault of theirs.
Detailed overview & validations of DPP4, put in vitro findings to physiological relevance. They act beyond the incretin subtrates by stablising the receptors while not interfering with GRH & IGF leading to untoward acromegaly.This is proved after sacrificing many innocent rats & dogs even as the brainy monkeys provided the keys to the men involved at the MSD Research and Development centre. The DPP4 inhibitors cause cleavage of multiple glucagon family of peptides. The incretin based therapies handle both defects of insulin resistance and insulin deficiency correcting islet (beta) cell dysfunction.
The advantages are-
- Minimal hypoglycemia - not driving the patient & physician to madness
- Preserving beta cell by increasing beta cell mass and preventing apoptosis
- Even regeneration of beta cells in the pancreatic duct has been demonstrated
- Still effectively reducing HbA1c
The triple mechanisms are -
- Reducing the hepatic glucose output
- Increasing insulin secretion
- Suppressing glucagon secretion.
The new AACE /ACE guide lines (table) give high priority to GLP1 agonist and DPP4 inhibitors.
The NICE guidelines on insulin therapy also recommend DPP4
Who wants the Gila monster's spit (exenatide) injections everyday with pain when the equally efficient orals are easily available,even though their prices may cause a hole in the pocket ?
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