We have demonstrated 1) that glucose levels saturate at levels above 75 mg in wildtype mice due to increase in insulin levels, 2) that GIP receptor KO mice have glucose intolerance after high glucose load due to insufficient increase in insulin levels, and 3) that GLP-1 receptor KO mice maintain glucose tolerance in spire of having GLP-1 receptor gene deletion due to a compensatory increase in insulin levels. The gene discussed is INS; the disease is Glucose intolerance.