Gastrointestinal (GI) disorders encompass a range of conditions affecting the GI tract, including dyspepsia, chronic inflammatory enteropathies (CIE), and malignant tumors. It is estimated that 6 to 60 billion cases of GI illness affect people worldwide each year. Both acute and chronic GI disorders in humans and animal models are characterized by an imbalance in redox homeostasis, which can be caused by either elevated reactive oxygen species (ROS) production or compromised antioxidant defense mechanisms. Oxidative stress (OS) is a recognized cause of GI disorders such as gastroduodenal ulcers, GI cancer, and CIE. There is a growing understanding that the endocrine system plays a role in the development and clinical progression of GI diseases through various mechanisms. Hormonal mechanisms exert a profound impact on various aspects of both immunological and inflammatory processes. Moreover, hormone receptors have been identified in reactive structures inside areas of inflammation, exhibiting a dual capacity to induce both pro- and anti-inflammatory responses. GI hormones, in addition to regulating secretion, absorption, digestion, and gut motility; also play a role in modulating maintenance of the GI mucosa and are implicated in the development of gut mucosal atrophy, neoplasms, and cancers. The pathophysiology of functional GI disorders involves changes in the gut microbiota/gut hormone axis, which significantly impact GI motility. A comprehensive grasp of the importance of hormones in GI diseases is imperative to elucidate the complex interplay between these variables and to discern potential strategies for addressing hormonally influenced GI symptoms/signs in patient subsets, such as women with IBD. The present research topic also addresses the primary endocrine manifestations associated with IBD/CIE, including but not limited to pubertal delay, hypogonadism, growth failure, and changes in lipid and carbohydrate metabolism.