While such surrogates for insulin sensitivity do show modest correlations with more direct measures of insulin sensitivity in animal models [25], in this case the particular anatomic and physiologic peculiarities of the GH transgenic mice (i.e., innate hyperinsulinemia putatively due to increased β-cell-to-body weight/size, as well as different body composition) might explain the divergence between surrogate measures and actual physiologic responses. This evidence concerns the gene GH1 and hyperinsulinism.