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PARP1, the most abundant and well-characterized family member, rapidly binds to DNA breaks and consumes large quantities of NAD+ to synthesize poly(ADP-ribose) chains that serve as recruitment platforms for DNA repair proteins

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as a result, the sequence homology of rodent and human GIPR is only 81%, and the effect of human GIP on rat and mouse GIPRs is only 75% and 60% of rat and mouse GIP, respectively

This does not prove that thicker blood caused these events, but it supports a plausible pathway involving restricted blood flow, a higher risk of clot formation, and greater strain on the heart