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Its effects on weight loss have been mixed, though

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GIP is the principal physiological incretin and plays a vital role in nutrient deposition and energy storage GIP exerts its physiological effects both directly by virtue of its insulin-mimetic properties and indirectly through its insulinotropic effects Enhanced postprandial secretion of GIP may initiate a vicious cycle characterized by increased nutrient uptake and storage in adipocytes, leading to insulin resistance and hyperinsulinemia Overexpression of GIP in obese individuals plays a major role in the pathogenesis of obesity, and it may exacerbate insulin resistance manifested by many patients with type 2 diabetes mellitus Despite the deleterious consequences of GIP overexpression, GIP analogues have been demonstrated to provide benefit in treating obesity by mechanisms currently not fully elucidated Preclinical studies have demonstrated that the abrogation of GIP signaling may potentially be useful in treating obesity and associated disorders Although often disregarded when considering nutrient homeostasis, the gastrointestinal (GI) tract, including hormones and other GI regulatory peptides in particular, must be regarded as an ideal starting point for such discussion since the GI tract represents the route by which all nutrients are ingested, processed, and absorbed