Diabetic Gastroparesis: Exploring the Role of Autonomic Neuropathy, Interstitial Cells of Cajal, and Emerging Prokinetic Agents

Patients with chronic diabetes mellitus commonly develop diabetic gastroparesis, an enduring gastrointestinal disorder. This condition can significantly affect patients' quality of life and is characterized by delayed gastric emptying without mechanical obstruction. Diabetes-related autonomic neuropathy, which impairs normal gastric motility and coordination, is the primary cause of this illness. Vagal nerve deterioration (autonomic neuropathy) that slows gastric emptying also affects the intestines in many long-term diabetics. As a result, bowel habits become irregular and highly sensitive, resembling IBS, while the gastrointestinal tract empties slowly (gastroparesis). This combination of upper-gastrointestinal (gastroparesis) and lower-gastrointestinal (IBS-type) symptoms occurs when blood sugar fluctuations also irritate the stomach. This review focuses on its origins, clinical signs and symptoms, diagnostic methods, and therapeutic approaches; it aims to provide a clear and thorough description of diabetic gastroparesis. The review discusses the development of gastroparesis in relation to interstitial cells of Cajal, persistent hyperglycemia, vagus nerve dysfunction, and altered gastric smooth muscle function. This review emphasizes prucalopride, a highly selective 5-HT4 receptor agonist, and pyridostigmine, and their relevance in treating diabetic gastroparesis.