Mice lacking GIP receptors [68] or K cells [69]were protected from obesity when fed a high-fat diet, and young prediabetic ob/ob mice treated with (Pro3) GIP a specific and stable GIP receptor antagonist prevented the development of diabetes and related metabolic abnormalities in these rodents [70] Therefore, GIP receptor antagonists, by opposing GIP's anabolic action on adipose tissue, could represent a new treatment modality for obesity [71]. This evidence concerns the gene GIP and obesity due to melanocortin 4 receptor deficiency.