Diabetic gastroparesis: pathophysiology and impact on insulin timing choices

Engineering notes

Key topics: autonomous driving, control. See the paper for implementation details and experimental results.

Chinese explanation / 中文解读

中文解读待补充：本站会优先为端到端自动驾驶、BEV感知、3D目标检测、轨迹预测、路径规划、LiDAR感知等高价值论文补充中文说明。

Original abstract

Diabetic gastroparesis (DGP) is a chronic and frequently underrecognized complication of diabetes mellitus, characterized by delayed gastric emptying in the absence of mechanical obstruction. It represents a clinically significant manifestation of diabetic autonomic neuropathy and arises from a complex interplay of sustained hyperglycemia, oxidative and nitrosative stress, advanced glycation end-product accumulation, impaired insulin/IGF-1 signaling, lipid dysmetabolism, and inflammatory activation. These mechanisms converge to damage autonomic and enteric neurons, reduce interstitial cells of Cajal density, and disrupt gastric smooth muscle function, ultimately leading to impaired and unpredictable gastric motility. Beyond gastrointestinal symptoms, DGP profoundly affects metabolic control. The altered timing and variability of gastric emptying disturb the physiological coordination between nutrient absorption and insulin pharmacokinetics, generating a temporal mismatch that predisposes patients to early postprandial hypoglycemia followed by late hyperglycemia. This pattern increases glycemic variability, complicates insulin dose adjustment, and contributes to oxidative stress and vascular risk. In this narrative review, we examine the current understanding of DGP pathophysiology and its clinical implications for insulin therapy. We discuss diagnostic strategies, nutritional interventions, and pharmacological treatments, with particular attention to insulin timing modulation. We also analyze the emerging role of diabetes technologies, including continuous glucose monitoring and automated insulin delivery systems, as well as future perspectives such as glucose-responsive insulins and regenerative approaches targeting gastric neuromuscular dysfunction. A mechanism-based, personalized therapeutic strategy may improve metabolic stability and patient outcomes.

Links and sources

• PDF from original source

Comments