Objective

Post–bariatric surgery hypoglycemia (PBH) is defined as the presence of neuroglycopenic symptoms accompanied by postprandial hypoglycemia in bariatric surgery patients. Recent clinical studies using continuous glucose monitoring (CGM) technology revealed that PBH is more frequently observed in vertical sleeve gastrectomy (VSG) patients than previously recognized. PBH cannot be alleviated by current medication. Therefore, a model system to investigate the mechanism and treatment is required.

Methods

We used CGM in a rat model of VSG and monitored the occurrence of glycemic variability and hypoglycemia in various meal conditions for 4 weeks after surgery. Another cohort of VSG rats with CGM was used to investigate whether the blockade of glucagon-like peptide-1 receptor (GLP-1R) signaling alleviates these symptoms. A mouse VSG model was used to investigate whether the impaired glucose counterregulatory system causes postprandial hypoglycemia.

Results

Like in humans, rats have increased glycemic variability and hypoglycemia after VSG. Postprandial hypoglycemia was specifically detected after liquid versus solid meals. Further, the blockade of GLP-1R signaling raises the glucose nadir but does not affect glycemic variability.

Conclusions

Rat bariatric surgery duplicates many features of human post–bariatric surgery hypoglycemia including postprandial hypoglycemia and glycemic variability, while blockade of GLP-1R signaling prevents hypoglycemia but not the variability.

中文翻译：

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连续的葡萄糖监测揭示了大鼠垂直袖胃切除术后的血糖变异性和低血糖。

客观的

aria门手术后低血糖症（PBH）的定义是，减肥手术患者中存在神经性血糖症状并伴有餐后低血糖症。最近使用连续葡萄糖监测（CGM）技术进行的临床研究表明，在垂直袖式胃切除术（VSG）患者中观察到PBH的频率比以前认识的要高。当前的药物无法缓解PBH。因此，需要一个模型系统来研究其机理和治疗方法。

方法

我们在VSG的大鼠模型中使用了CGM，并在术后4周内监测了各种进餐条件下血糖变异性和低血糖的发生。另一项VSG大鼠与CGM队列用于研究胰高血糖素样肽1受体（GLP-1R）信号传导的阻滞是否减轻了这些症状。小鼠VSG模型用于研究受损的葡萄糖反调节系统是否引起餐后低血糖。

结果

与人类一样，VSG后大鼠的血糖变异性和低血糖增加。相对于固体餐而言，餐后低血糖是专门检测出来的。此外，对GLP-1R信号传导的阻断提高了葡萄糖最低点，但不影响血糖变异性。

结论

大鼠减肥手术复制了人类b门手术后低血糖的许多特征，包括餐后低血糖和血糖变异性，而阻断GLP-1R信号传导可以预防低血糖症，但不能阻止变异性。