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Duodenum cells refer to the diverse cellular populations within the first segment of the small intestine, including absorptive enterocytes, mucus-secreting goblet cells, and various hormone-producing enteroendocrine cells [6, 7]. These cells are primarily responsible for the neutralization of acidic gastric chyme through bicarbonate secretion from Brunner's glands and the chemical digestion of nutrients through the reception of pancreatic and biliary secretions [8, 22]. Enteroendocrine cells within the duodenal mucosa, such as I-cells, S-cells, K-cells, and L-cells, secrete critical hormones including cholecystokinin (CCK), secretin, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1), which together regulate appetite, gastric emptying, and systemic glucose homeostasis [2, 15, 16]. While the duodenum is a tissue/cell collection rather than a single molecular target, it hosts numerous receptors and transporters targeted by drugs, such as the GLP-1 receptor for diabetes and H2 receptors for acid suppression [18, 23]. Pathological states like Celiac disease involve the destruction of duodenal enterocytes, while chronic inflammation can lead to peptic ulcers or duodenal adenocarcinoma [13, 14, 22]. Modern therapeutic approaches, such as duodenal mucosal resurfacing (DMR), target the duodenal lining to treat metabolic disorders like type 2 diabetes and obesity [5, 12].
Drugs act on these cells by targeting specific intracellular enzymes (e.g., H+/K+ ATPase), surface receptors (e.g., H2, GLP-1R), or nutrient transporters (e.g., SGLT1); additionally, mucosal resurfacing involves thermal ablation of the hypertrophied duodenal cell layer to restore metabolic signaling [2, 5, 20, 23].
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