An important difference however between the 2 models is that supraphysiological hyperinsulinemia is induced in the EHC model using exogenous insulin, whereas the endogenous hyperinsulinemia induced in the PGI model (by an IV glucose infusion) is comparable to that observed in naturally occurring cases of hyperinsulinemia‐associated laminitis.1 Here, INS is linked to Hyperinsulinemia.