Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, 1008 West Hazelwood Drive, Urbana, IL 61802, USA.
Domest Anim Endocrinol. 2011 May;40(4):205-12. doi: 10.1016/j.domaniend.2011.01.002. Epub 2011 Feb 24.
Incretin hormones are secreted from the intestines in response to specific nutrients. They potentiate insulin secretion and have other beneficial effects in glucose homeostasis. We aimed to study the incretin effect in cats and to compare the effect of oral glucose, lipids, or amino acids on serum concentrations of insulin, total glucose-dependent insulinotropic peptide (GIP) and total glucagon-like peptide 1 (GLP-1). Ten healthy cats were used in a repeated measures design. Glucose, lipid, or amino acids were administered through nasoesophageal tubes on separate days. Blood glucose (BG) concentrations were matched between experiments by measuring BG every 5 min and infusing glucose intravenously at a changing rate. Intravenous glucose infusion with no prior treatment served as control. The incretin effect was estimated as the difference in insulin area under the curve (AUC) after oral compared with intravenous glucose. Temporal changes and total amount of hormone secretions were compared between treatment groups with the use of mixed models. Total glucose infused (TGI) at a mean dose of 0.49 g/kg resulted in slightly higher BG compared with 1 g/kg oral glucose (P = 0.038), but insulin concentrations were not significantly different (P = 0.367). BG and the TGI were not significantly different after the 3 oral challenges. Total GIP AUC was larger after lipids compared with amino acids (P = 0.0012) but GIP concentrations did not increase after oral glucose. Insulin and GIP concentrations were positively correlated after lipid (P < 0.001) and amino acids (P < 0.001) stimulations, respectively, but not after oral glucose stimulation. Total GLP-1 AUC was similar after all three oral stimulations. Insulin and GLP-1 concentrations were positively correlated after glucose (P = 0.001), amino acids (P < 0.001), or lipids (P = 0.001) stimulations. Our data indirectly support an insulinotropic effect of GIP and GLP-1. Potentiation of insulin secretion after oral glucose is minimal in cats and is mediated by GLP-1 but not GIP.
肠促胰岛素激素是响应特定营养素从肠道分泌的。它们增强胰岛素分泌,并在葡萄糖稳态中有其他有益作用。我们旨在研究猫的肠促胰岛素效应,并比较口服葡萄糖、脂质或氨基酸对血清胰岛素、总葡萄糖依赖性胰岛素释放肽(GIP)和总胰高血糖素样肽 1(GLP-1)浓度的影响。10 只健康猫采用重复测量设计。在不同的日子里,通过鼻胃管给予葡萄糖、脂质或氨基酸。通过每 5 分钟测量血糖(BG)浓度并以变化的速率静脉内输注葡萄糖来使实验之间的 BG 浓度匹配。静脉内输注无预处理的葡萄糖作为对照。口服与静脉内葡萄糖相比,胰岛素曲线下面积(AUC)的差异估计为肠促胰岛素效应。使用混合模型比较治疗组之间激素分泌的时间变化和总量。以 0.49 g/kg 的平均剂量输注总葡萄糖(TGI)导致 BG 略高于 1 g/kg 口服葡萄糖(P = 0.038),但胰岛素浓度无显著差异(P = 0.367)。在 3 次口服挑战后,BG 和 TGI 没有显著差异。与氨基酸相比,脂质后总 GIP AUC 更大(P = 0.0012),但口服葡萄糖后 GIP 浓度没有增加。脂质(P < 0.001)和氨基酸(P < 0.001)刺激后胰岛素和 GIP 浓度呈正相关,但口服葡萄糖刺激后则不然。所有 3 次口服刺激后总 GLP-1 AUC 相似。葡萄糖(P = 0.001)、氨基酸(P < 0.001)或脂质(P = 0.001)刺激后,胰岛素和 GLP-1 浓度呈正相关。我们的数据间接支持 GIP 和 GLP-1 的胰岛素促分泌作用。猫口服葡萄糖后胰岛素分泌的增强作用很小,由 GLP-1 介导,但不由 GIP 介导。