INS and Hyperglycemia: Thus, the original Nidd2n, which was mapped to a relatively broad region in the middle portion of Chr 14 [6], is now dissected into multiple components: Nidd2.1n in the most proximal segment of NSY-Chr 14, retained in R2 and contributing to hyperglycemia, insulin resistance and adiposity; Nidd2.2n in the distal segment of NSY-Chr 14, retained in R0 but not in R1, for insulin resistance and hyperglycemia; and Adp1n in the middle segment of NSY-Chr 14, retained in R1 but not in R2, reducing adiposity and improving insulin sensitivity (Figure 4).