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孕期蛋白质限制可损害胰岛内 GLP-1 及β细胞质量的扩增。

Protein restriction during pregnancy impairs intra-islet GLP-1 and the expansion of β-cell mass.

机构信息

Mestrado em Nutrição, Alimentos e Metabolismo, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil.

Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil.

出版信息

Mol Cell Endocrinol. 2020 Dec 1;518:110977. doi: 10.1016/j.mce.2020.110977. Epub 2020 Aug 11.

DOI:10.1016/j.mce.2020.110977
PMID:32791189
Abstract

We evaluated whether protein restriction during pregnancy alters the morphometry of pancreatic islets, the intra-islet glucagon-like peptide-1 (GLP-1) production, and the anti-apoptotic signalling pathway modulated by GLP-1. Control non-pregnant (CNP) and control pregnant (CP) rats were fed a 17% protein diet, and low-protein non-pregnant (LPNP) and low-protein pregnant (LPP) groups were fed a 6% protein diet. The masses of islets and β-cells were similar in the LPNP group and the CNP group but were higher in the CP group than in the CNP group and were equal in the LPP group and the LPNP group. Both variables were lower in the LPP group than in the CP group. Prohormone convertase 2 and GLP-1 fluorescence in α-cells was lower in the low-protein groups than in the control groups. The least PC2/glucagon colocalization was observed in the LPP group, and the most was observed in the CP group. There was less prohormone convertase 1/3/glucagon colocalization in the LPP group than in the CP group. GLP-1/glucagon colocalization was similar in the LPP, CP and CNP groups, which showed less GLP-1/glucagon colocalization than the LPNP group. The mRNA Pka, Creb and Pdx-1 contents were higher in islets from pregnant rats than in islets from non-pregnant rats. Protein restriction during pregnancy impaired the mass of β-cells and the intra-islet GLP-1 production but did not interfere with the transcription of genes of the anti-apoptotic signalling pathway modulated by GLP-1.

摘要

我们评估了孕期蛋白质限制是否会改变胰岛的形态计量学、胰岛内胰高血糖素样肽-1(GLP-1)的产生以及 GLP-1 调节的抗凋亡信号通路。对照组非妊娠(CNP)和对照组妊娠(CP)大鼠给予 17%蛋白质饮食,低蛋白非妊娠(LPNP)和低蛋白妊娠(LPP)组给予 6%蛋白质饮食。LPNP 组和 CNP 组的胰岛和β细胞质量相似,但 CP 组高于 CNP 组,LPP 组与 LPNP 组相同。LPP 组的这两个变量均低于 CP 组。低蛋白组的前激素转化酶 2 和 GLP-1 在α细胞中的荧光低于对照组。LPP 组观察到的 PC2/胰高血糖素共定位最少,CP 组观察到的最多。LPP 组的前激素转化酶 1/3/胰高血糖素共定位少于 CP 组。LPP、CP 和 CNP 组的 GLP-1/胰高血糖素共定位相似,均低于 LPNP 组。与非妊娠大鼠相比,妊娠大鼠胰岛中的 Pka、Creb 和 Pdx-1 mRNA 含量更高。孕期蛋白质限制损害了β细胞的质量和胰岛内 GLP-1 的产生,但不干扰 GLP-1 调节的抗凋亡信号通路的基因转录。

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