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 vascular endothelial growth factor-A (Vegfa), vascular endothelial growth factor receptor 1 (Flt1), and Neuropilin1 (Nrp1). 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.
Highlights
Elevated postprandial blood triglyceride (TG) concentrations, which are mainly caused by an increase in chylomicron (CM) production, are considered a causal risk factor for low-grade inflammation and atherosclerotic cardiovascular disease [1,2]
We examined the secretion of apolipoproteins, including apoA-I, apolipoprotein A-IV (apoA-IV), We examined the secretion of apolipoproteins, including apoA-I, apoAapoB-48, and rat mucosal mast cell protease II (RMCPII)
We found that there were significantly increased l various lipids (TG, CHOL, PL, and NEFA) and apolipoprotein output in the of various lipids
Summary
Elevated postprandial blood triglyceride (TG) concentrations, which are mainly caused by an increase in chylomicron (CM) production, are considered a causal risk factor for low-grade inflammation and atherosclerotic cardiovascular disease [1,2]. The sequential meal pattern has received more attention, since previous studies have mainly focused on the single-meal effect on nutrient absorption and related metabolism, which is physiologically not reflective of the scenario in human feeding. Dietary fat (mainly in the form of TG) is hydrolyzed into fatty acids (FAs), glycerol, and monoglycerides by pancreatic lipase in the intestinal lumen [4]. These digestive products are taken up by the enterocytes, where the majority of re-esterified TG is packaged to assemble CMs and secreted into circulation via the lymphatic system. A certain amount of lipids may be stored in the enterocytes and form cytoplasmic lipid droplets (CLDs)
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