In its severe form, obesity can further manifest to the pathology of type 2 diabetes, including elevated glucose and insulin in fasting individuals, lower insulin‐receptor activity, delayed blood glucose clearance (a poor glucose‐tolerance response), and increased glucose–insulin by‐products, as measured by the homeostatic model assessment of insulin resistance (reviewed in ref. 41, 42). This evidence concerns the gene INS and type 2 diabetes mellitus.