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Although not entirely known, the mechanism(s) of elevation of GGT activity in patients with chronic liver disease of various etiologies may involve not only a passive release of the enzyme from the injured cells but also an accelerated release kinetics due to either increased intracellular synthesis or enhanced release into the bloodstream of GGT molecules expressed on cell surface [19]
It is more potent at GIP receptors than natural GIP, while maintaining carefully calibrated activity at GLP-1 and glucagon receptors
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