Stereospecific effects of fatty acids on proglucagon-derived peptide secretion in fetal rat intestinal cultures.
Stereospecific effects of fatty acids on proglucagon-derived peptide secretion in fetal rat intestinal cultures.
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脂肪酸对胎鼠肠道培养物中胰高血糖素原衍生肽分泌的立体特异性影响。
DOI：
10.1210/endo.136.12.7588313
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发表时间：
1995
期刊：
影响因子：
4.8
通讯作者：
P. Brubaker
中科院分区：
文献类型：
--
作者：
A. Rocca;P. Brubaker
脂肪的摄入是对胰高血糖素原衍生肽（PGDP）的分泌的有力刺激，包括来自肠L细胞的促胰岛素肽胰高血糖素样肽-1。该研究的目的是表征脂肪酸诱导的PGDP分泌的结构要求，并研究脂肪酸介导PGDP分泌的细胞机制。将胎鼠肠细胞培养物与10-150 μ M脂肪酸一起孵育，脂肪酸的链长（14-18个碳）和不饱和度（0-2）不同。蛋白激酶C（PKC）和脂肪酸酯化和氧化的抑制剂也与细胞在刺激性脂肪酸的存在下孵育。测定培养物的胰高血糖素样免疫反应性和胰高血糖素样肽-1-（7-36）NH 2分泌。链长大于14个碳的单不饱和脂肪酸以剂量依赖性方式刺激PGDP分泌1.8至3.4倍（P < 0.05至P < 0.001）。增强的PGDP分泌在刺激性脂肪酸完全饱和后丧失。此外，虽然封锁脂肪酸酯化与羧基甲基酯基团阻止PGDP分泌，抑制脂肪酸氧化与甲基palmoxirate没有阻止PGDP分泌。最后，使用各种PKC抑制剂（staurosporine，H7，24小时下调）也没有改变脂肪酸诱导的PGDP分泌。总之，具有游离羧基的单不饱和长链脂肪酸刺激肠道PGDP分泌。无论是脂肪酸氧化还是经典的PKC亚型似乎直接参与这种反应。因此，脂肪酸的结构在诱导肠道PGDP分泌中起着核心作用。这些发现表明，脂肪组成可能会显著影响GLP-1对摄入营养素的反应程度。
The ingestion of fats is a potent stimulus for the secretion of the proglucagon-derived peptides (PGDPs), including the insulinotropic peptide glucagon-like peptide-1 from the intestinal L cell. The aim of the study was to characterize the structural requirements for fatty acid-induced secretion of the PGDPs and investigate the cellular mechanisms through which fatty acids mediate PGDP secretion. Fetal rat intestinal cell cultures were incubated with 10-150 microM fatty acids that differed in chain length (14-18 carbons) and degree of unsaturation (0-2). Inhibitors of protein kinase C (PKC) and fatty acid esterification and oxidation were also incubated with the cells in the presence of stimulatory fatty acids. The cultures were assayed for glucagon-like immunoreactivity and glucagon-like peptide-1-(7-36)NH2 secretion. Monounsaturated fatty acids of chain length greater than 14 carbons stimulated PGDP secretion by 1.8 to 3.4-fold in a dose-dependent fashion (P < 0.05 to P < 0.001). Enhanced PGDP secretion was lost upon full saturation of the stimulatory fatty acids. Furthermore, although blockade of fatty acid esterification with a carboxyl methyl ester group prevented PGDP secretion, inhibition of fatty acid oxidation with methyl palmoxirate did not prevent PGDP secretion. Finally, the use of various inhibitors of PKC (staurosporine, H7, 24-h down-regulation) also did not alter fatty acid-induced PGDP secretion. In conclusion, monounsaturated long-chain fatty acids possessing a free carboxyl group stimulate intestinal PGDP secretion. Neither fatty acid oxidation nor classical isoforms of PKC appear to be directly involved in this response. Therefore, the structure of the fatty acid plays a central role in inducing intestinal PGDP secretion. These findings suggest that fat composition may significantly affect the magnitude of the GLP-1 response to ingested nutrients.
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