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序贯脂质餐对大鼠淋巴脂质吸收和转运的影响。

Impact of Sequential Lipid Meals on Lymphatic Lipid Absorption and Transport in Rats.

机构信息

Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA.

Department of Medicine and Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

Genes (Basel). 2022 Jan 30;13(2):277. doi: 10.3390/genes13020277.

DOI:10.3390/genes13020277
PMID:35205322
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8871868/
Abstract

The sequential meal pattern has recently received more attention because it reflects a phycological diet style for human beings. The present study investigated the effects of the second lipid meal on lymphatic lipid absorption and transport in adult rats following a previous lipid meal. Using the well-established lymph fistula model, we found that the second lipid meal significantly increased the lymphatic output of triglycerides, cholesterol, phospholipids, and non-esterified fatty acids compared with a single lipid meal. Besides that, the time reaching the peak of each lipid output was significantly faster compared with the first lipid meal. Additionally, the second lipid meal significantly increased the lymphatic output of apolipoprotein A-IV (ApoA-IV), but not apolipoprotein B-48 (ApoB-48) or apolipoprotein A-I (ApoA-I). Interestingly, the triglyceride/apoB-48 ratio was significantly increased after the second lipid meal, indicating the increased chylomicron size in the lymph. Finally, the second lipid meal increased the lymphatic output of rat mucosal mast cell protease II (RMCPII). No change was found in the expression of genes related to the permeability of lymphatic lacteals, including (), (), (). Collectively, the second lipid meal led to the rapid appearance of bigger-sized chylomicrons in the lymph. It also increased the lymphatic output of various lipids and apoA-IV, and mucosal mast cell activity in the intestine.

摘要

序贯进食模式最近受到了更多关注,因为它反映了人类的一种心理饮食方式。本研究探讨了在先前的脂质餐后,第二餐脂质对成年大鼠淋巴脂质吸收和转运的影响。使用成熟的淋巴瘘模型,我们发现与单一脂质餐相比,第二餐脂质显著增加了甘油三酯、胆固醇、磷脂和非酯化脂肪酸的淋巴输出。此外,与第一餐脂质相比,每种脂质输出达到峰值的时间明显更快。此外,第二餐脂质显著增加了载脂蛋白 A-IV(ApoA-IV)的淋巴输出,但载脂蛋白 B-48(ApoB-48)或载脂蛋白 A-I(ApoA-I)没有增加。有趣的是,第二餐脂质后,甘油三酯/载脂蛋白 B-48 比值显著增加,表明淋巴中乳糜微粒的大小增加。最后,第二餐脂质增加了大鼠黏膜肥大细胞蛋白酶 II(RMCPII)的淋巴输出。与乳糜淋巴管通透性相关的基因表达没有变化,包括 ()、 ()、 ()。总之,第二餐脂质导致更大尺寸的乳糜微粒迅速出现在淋巴中。它还增加了各种脂质和 apoA-IV 以及肠道黏膜肥大细胞活性的淋巴输出。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/471c5a9408d5/genes-13-00277-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/5f25947026e5/genes-13-00277-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/6567f409baef/genes-13-00277-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/66ab1eb23de4/genes-13-00277-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/87c8841994bb/genes-13-00277-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/cca15c3d46a8/genes-13-00277-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/d93b4ecdc528/genes-13-00277-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/4c0d0f0d400b/genes-13-00277-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/471c5a9408d5/genes-13-00277-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/5f25947026e5/genes-13-00277-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/6567f409baef/genes-13-00277-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/66ab1eb23de4/genes-13-00277-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/87c8841994bb/genes-13-00277-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/cca15c3d46a8/genes-13-00277-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/d93b4ecdc528/genes-13-00277-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/4c0d0f0d400b/genes-13-00277-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5071/8871868/471c5a9408d5/genes-13-00277-g008.jpg

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本文引用的文献

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Human intestinal lipid storage through sequential meals reveals faster dinner appearance is associated with hyperlipidemia.通过连续进餐观察人类肠道脂质储存发现,晚餐更快出现与高脂血症有关。
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Glucose and GLP-2 (Glucagon-Like Peptide-2) Mobilize Intestinal Triglyceride by Distinct Mechanisms.葡萄糖和 GLP-2(胰高血糖素样肽-2)通过不同的机制动员肠道甘油三酯。
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