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The peptides, based on GIP 1-42 include substitutions and/or modifications which have enhanced resistance to degradation by the enzyme dipeptidyl peptidase IV (DPP IV). GIP acts through binding to specific G-protein coupled GIP receptors located on pancreatic beta-cells (Wheeler, M. Several attempts have been made to produce structurally modified analogues of t GLP-1 which are resistant to DPP IV degradation. Thus in these transgenic mice, life-long depletion of GIP-R function was associated with decreased body weight gain and significant amelioration of both adiposity and insulin resistance compared with control (Lep) mice (Miyawaki, K. Synthesis of GIP and N-terminally modified GIP analogues.

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