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

Figure 1 Brain-gut axis dysfunction and core cascade in diabetic gastroparesis. Chronic hyperglycemia-driven oxidative stress/inflammation disrupts central nervous system-autonomic nervous system-enteric nervous system regulation and the enteric nervous system-interstitial cells of Cajal-smooth muscle network, leading to pyloric/antral dysmotility and delayed gastric emptying. Bidirectional feedback among immune activation, neural injury, and gut dysbiosis contributes to symptom heterogeneity with a limited symptom-emptying correlation. ANS: Autonomic nervous system; DMV: Dorsal motor nucleus of the vagus; ENS: Enteric nervous system; ICC: Interstitial cells of Cajal; IL-6: Interleukin-6; LPS: Lipopolysaccharides; NO: Nitric oxide; nNOS: Neuronal nitric oxide synthase; NTS: Nucleus tractus solitarius; ROS: Reactive oxygen species; SCFAs: Short chain fatty acids; TNF-α: Tumor necrosis factor-α; 5-HT: 5-hydroxytryptamine. Created in BioRender (Supplementary material).