Type 2 diabetes mellitus (T2DM) is a major global health challenge, primarily driven by the body’s impaired ability to effectively utilize insulin. The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) play essential roles in regulating glucose metabolism. GIP, an intestinal hormone, exerts a wide range of physiological effects, including the promotion of insulin secretion following meals and the stimulation of glucagon release under euglycemic and hypoglycemic conditions. Moreover, GIP facilitates triacylglycerol absorption in adipose tissue and reduces bone resorption. Numerous GLP-1 receptor agonists and dual GIP/GLP-1 receptor agonists have been developed to harness these hormonal benefits for T2DM treatment. Some of these therapies have demonstrated notable success in managing weight and reducing cardiovascular disease risk. A deeper understanding of cellular and molecular pathways underlying these effects holds promise for developing next-generation incretin-based therapies with enhanced efficacy and fewer adverse effects. Although numerous studies have targeted the GLP-1 receptor for T2DM management, the therapeutic potential of the GIP receptor (GIPR) remains under investigation. Despite emerging evidence linking GIP to key mechanisms in T2DM pathophysiology, its full clinical utility has yet to be determined. This article explores GIP’s potential as a therapeutic target for T2DM, examining its role in regulating pancreatic α-and β-cell function, adipose tissue dynamics, bone remodeling, lipid metabolism, cardiovascular disease, and kidney disorders. It also evaluates the therapeutic potential of both GIPR agonists and antagonists, illustrating how these approaches may enhance the understanding of GIP’s relevance in T2DM management. Additionally, this discussion addresses challenges associated with translating GIP-targeted therapies into clinical practice, offering insights into overcoming existing barriers and advancing more comprehensive treatment options.