Dietary resistant starch upregulates total GLP-1 and PYY in a sustained day-long manner through fermentation in rodents

Dietary resistant starch upregulates total GLP-1 and PYY in a sustained day-long manner through fermentation in rodents
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DOI:
10.1152/ajpendo.90637.2008
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发表时间:
2008-11-01
影响因子:
5.1
通讯作者:
Keenan, Michael J.
Keenan, Michael J.
中科院分区:
医学2区
文献类型:
--
作者:
Zhou, June;Martin, Roy J.;Keenan, Michael J.

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首页--期刊主要分类--期刊细介绍--期刊题录与文摘--期刊详细文摘内容饮食抗性淀粉在啮齿动物体内持续一天的发酵过程中上调总GLP-1和PYY。AM J生理学内分泌代谢酶295:E1160-E1166,2008。首次发表于2008年9月16日;DOI:10.1152/ajpendo.90637.2008.GLP-1(GLP-1)和YY(PYY)是餐后从肠道分泌的抗糖尿病/肥胖荷尔蒙。我们已经表明,膳食抗性淀粉(RS)增加了GLP-1和PYY的分泌,但其机制尚不清楚。RS是一种可发酵的纤维,可降低饮食的血糖指数,并通过肠道发酵释放短链脂肪酸(SCFAs)。这项研究探讨了RS刺激GLP-1和PYY分泌的两种可能机制:一餐或血糖指数的影响,以及发酵的影响。由于GLP-1和PYY的分泌受到肠道营养可获得性的刺激,因此当比较两种不同血糖指数的饮食时,血液样本采集的时机可能会影响结果。因此,我们检测了RS喂养的大鼠24小时内不同时间点的GLP-1和PYY血浆水平。此外,我们在体外检测了RS喂养的大鼠肠道的特定区域以及暴露于SCFA后的肠内分泌细胞系中的前高血糖素(GLP-1的前体)和PYY基因的表达模式。我们的研究结果如下。1)RS以一整天的方式刺激GLP-1和PYY的分泌,与膳食效应或饮食血糖的变化无关。2)低位肠道中单链脂肪酸的发酵和释放与胰升糖素原和PYY基因表达的增加有关。3)糖耐量(GLP-1和PYY活性形式增加的指标)在RS喂养的糖尿病小鼠中得到改善。我们认为RS的发酵很可能是啮齿动物内源性总GLP-1和PYY分泌增加的主要机制。因此,在使用日粮可发酵纤维刺激GLP-1和PYY分泌时,应考虑任何影响发酵的因素。
Zhou J, Martin RJ, Tulley RT, Raggio AM, McCutcheon KL, Shen L, Danna SC, Tripathy S, Hegsted M, Keenan MJ. Dietary resistant starch upregulates total GLP-1 and PYY in a sustained day-long manner through fermentation in rodents. Am J Physiol Endocrinol Metab 295: E1160-E1166, 2008. First published September 16, 2008; doi:10.1152/ajpendo.90637.2008.-Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are anti-diabetes/obesity hormones secreted from the gut after meal ingestion. We have shown that dietary-resistant starch (RS) increased GLP-1 and PYY secretion, but the mechanism remains unknown. RS is a fermentable fiber that lowers the glycemic index of the diet and liberates short-chain fatty acids (SCFAs) through fermentation in the gut. This study investigates the two possible mechanisms by which RS stimulates GLP-1 and PYY secretion: the effect of a meal or glycemic index, and the effect of fermentation. Because GLP-1 and PYY secretions are stimulated by nutrient availability in the gut, the timing of blood sample collections could influence the outcome when two diets with different glycemic indexes are compared. Thus we examined GLP-1 and PYY plasma levels at various time points over a 24-h period in RS-fed rats. In addition, we tested proglucagon (a precursor to GLP-1) and PYY gene expression patterns in specific areas of the gut of RS-fed rats and in an enteroendocrine cell line following exposure to SCFAs in vitro. Our findings are as follows. 1) RS stimulates GLP-1 and PYY secretion in a substantial day-long manner, independent of meal effect or changes in dietary glycemia. 2) Fermentation and the liberation of SCFAs in the lower gut are associated with increased proglucagon and PYY gene expression. 3) Glucose tolerance, an indicator of increased active forms of GLP-1 and PYY, was improved in RS-fed diabetic mice. We conclude that fermentation of RS is most likely the primary mechanism for increased endogenous secretions of total GLP-1 and PYY in rodents. Thus any factor that affects fermentation should be considered when dietary fermentable fiber is used to stimulate GLP-1 and PYY secretion.