Gastric bypass surgery enhances glucagon-like peptide 1-stimulated postprandial insulin secretion in humans.
Gastric bypass surgery enhances glucagon-like peptide 1-stimulated postprandial insulin secretion in humans.
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DOI：
10.2337/db11-0203
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发表时间：
2011-09
期刊：
影响因子：
7.7
通讯作者：
D'Alessio DA
中科院分区：
文献类型：
--
作者：
Salehi M;Prigeon RL;D'Alessio DA
胃绕道（GB）手术与餐后高胰岛素血症有关，这种影响在术后出现反复低血糖的患者中更为明显。 GB 后肠促胰岛素胰高血糖素样肽 1 (GLP-1) 的血浆水平显着升高，表明其作用有助于改变餐后血糖调节。本研究的目的是确定 GLP-1 对 GB 患者胰岛素分泌的作用。 12 名既往患有 GB 的无症状个体 (Asym-GB)、10 名匹配的健康未手术对照受试者以及 12 名 GB 后复发性低血糖患者 (Hypo-GB) 在使用 Exendin-(9-39) 或生理盐水阻断 GLP-1 受体的高血糖钳夹过程中测量了餐前和餐后激素水平和胰岛素分泌率 (ISR)。与对照受试者相比，阻断 GLP-1 的作用可在更大程度上抑制 Asym-GB 个体的餐后 ISR（33 ± 4 vs.16 ± 5%；P = 0.04）。在 Hypo-GB 患者中，GLP-1 占餐后 ISR 的 43 ± 4%，这并不显着高于 Asym-GB 受试者（P = 0.20）。所有组中胰高血糖素均受到高血糖的类似抑制，但手术个体餐后胰高血糖素显着升高，但在非手术受试者中仍受到抑制。 GLP-1 受体阻断增加了两个手术组的餐后胰高血糖素。 GLP-1 刺激的胰岛素分泌增加显着导致 GB 受试者胰岛素过多症。然而，GLP-1 对手术受试者餐后胰岛素分泌的夸大影响在有或没有反复低血糖的受试者中没有显着差异。
Gastric bypass (GB) surgery is associated with postprandial hyperinsulinemia, and this effect is accentuated in postsurgical patients who develop recurrent hypoglycemia. Plasma levels of the incretin glucagon-like peptide 1 (GLP-1) are dramatically increased after GB, suggesting that its action contributes to alteration in postprandial glucose regulation. The aim of this study was to establish the role of GLP-1 on insulin secretion in patients with GB. Twelve asymptomatic individuals with previous GB (Asym-GB), 10 matched healthy nonoperated control subjects, and 12 patients with recurrent hypoglycemia after GB (Hypo-GB) had pre- and postprandial hormone levels and insulin secretion rates (ISR) measured during a hyperglycemic clamp with either GLP-1 receptor blockade with exendin-(9–39) or saline. Blocking the action of GLP-1 suppressed postprandial ISR to a larger extent in Asym-GB individuals versus control subjects (33 ± 4 vs.16 ± 5%; P = 0.04). In Hypo-GB patients, GLP-1 accounted for 43 ± 4% of postprandial ISR, which was not significantly higher than that in Asym-GB subjects (P = 0.20). Glucagon was suppressed similarly by hyperglycemia in all groups but rose significantly after the meal in surgical individuals but remained suppressed in nonsurgical subjects. GLP-1 receptor blockade increased postprandial glucagon in both surgical groups. Increased GLP-1–stimulated insulin secretion contributes significantly to hyperinsulinism in GB subjects. However, the exaggerated effect of GLP-1 on postprandial insulin secretion in surgical subjects is not significantly different in those with and without recurrent hypoglycemia.