Dysfunction of the brain-gut axis in diabetic gastroparesis: Underlying mechanisms and therapeutic strategies

Table 1 Phenotype-oriented pharmacological strategies targeting the brain-gut axis in diabetic gastroparesis

Patient phenotype	Dominant pathophysiological features	Representative agents	Therapeutic focus
Central-dominant phenotype	Central sensory integration and regulatory dysfunction, with symptom severity disproportionate to DGE	Metoclopramide; aprepitant	Predominantly central modulation to alleviate nausea and vomiting and improve brain-gut signal processing
Peripheral neuro-effector-dominant phenotype	Enteric nervous system and interstitial cells of Cajal injury with impaired antral motility and pyloric dysfunction, associated with marked DGE	Domperidone; erythromycin; azithromycin; ulimorelin (TZP-101/102); relamorelin (RM-131); mosapride; prucalopride	Enhancement of peripheral neuromuscular function to restore gastric rhythmicity and accelerate gastric emptying
Inflammation-microbiota-associated phenotype	Low-grade inflammation, oxidative stress, and gut microbiota dysbiosis	Alpinia officinarum extract; FoxiangSan; Salsola collina ethyl acetate extract; amomum compactum volatile oil; curcumin; berberine; plant-derived serotonin	Modulation of inflammatory responses and gut microbiota to improve overall brain-gut axis homeostasis

DGE: Delayed gastric emptying.