scholarly journals Monosodium glutamate inhibits the lymphatic transport of lipids in the rat

2016 ◽  
Vol 311 (4) ◽  
pp. G648-G654 ◽  
Author(s):  
Alison B. Kohan ◽  
Qing Yang ◽  
Min Xu ◽  
Dana Lee ◽  
Patrick Tso
Keyword(s):  
Continuous Infusion ◽  
Intestinal Mucosa ◽  
Lipid Emulsion ◽  
Monosodium Glutamate ◽  
Dietary Lipids ◽  
Intestinal Lumen ◽  
Lymphatic Transport ◽  
Gastrointestinal Physiology ◽  
Cholesterol Secretion

It is not well understood how monosodium glutamate (MSG) affects gastrointestinal physiology, especially regarding the absorption and the subsequent transport of dietary lipids into lymph. Thus far, there is little information about how the ingestion of MSG affects the lipid lipolysis, uptake, intracellular esterification, and formation and secretion of chylomicrons. Using lymph fistula rats treated with the infusion of a 2% MSG solution before a continuous infusion of triglyceride, we show that MSG causes a significant decrease in both triglyceride and cholesterol secretion into lymph. Intriguingly, the diminished lymphatic transport of triglyceride and cholesterol was not caused by an accumulation of these labeled lipids in the intestinal lumen or in the intestinal mucosa. Rather, it is a result of increased portal transport in the animals fed acutely the lipid plus 2% MSG in the lipid emulsion. This is a first demonstration of MSG on intestinal lymphatic transport of lipids.

Effect of hydrophobic surfactant (Pluronic L-81) on lymphatic lipid transport in the rat

1980 ◽  
Vol 239 (5) ◽  
pp. G348-G353 ◽  
Author(s):  
P. Tso ◽  
J. A. Balint ◽  
J. B. Rodgers
Keyword(s):  
Thoracic Duct ◽  
Lipid Emulsion ◽  
Sodium Taurocholate ◽  
Lipid Transport ◽  
Intestinal Lumen ◽  
Lymphatic Transport ◽  
Lipid Fractions ◽  
Mucosal Cells ◽  
Marked Accumulation ◽  
Lipoprotein Assembly

The effect of chronic feeding (3-4 wk) of the hydrophobic surfactant, Pluronic L-81, on the lymphatic transport of triglyceride and cholesterol was studied in rats with thoracic duct fistula. A lipid emulsion containing [3H]triolein (13.3 mM), [14C]cholesterol (2.6 mM), phosphatidylcholine (2.9 mM), sodium taurocholate (19 mM), with 0.17 mg/ml (experimental) or without Pluronic L-81 (L-81) added (control) was infused at the rate of 3 ml/h. Lymph triglyceride and cholesterol outputs were greatly impaired in the experimental rats compared to the control rats. The phospholipid output compared to the control was also reduced but to a lesser extent in the experimental rats. Comparable recovery of radioactive 3H-labeled lipid and [14C]cholesterol from the intestinal lumen of control and experimental rats showed that digestion and absorption were not impaired in the experimental rats. The distribution of mucosal 3H radioactivity in various lipid fractions showed no impairment in reesterification. The greatly depressed lymphatic lipid transport was associated with marked accumulation of absorbed lipid in enterocytes, suggesting that Pluronic L-81 interferes with lipoprotein assembly and/or exit of lipoproteins from the mucosal cells. The animals fed chronically for 4-6 wk regained their ability to transport lipid 24 h after termination of L-81 feeding. The effect of this agent, therefore, is readily reversible.

scholarly journals Apolipoprotein A-V deficiency enhances chylomicron production in lymph fistula mice

2015 ◽  
Vol 308 (7) ◽  
pp. G634-G642 ◽  
Author(s):  
Linda S. Zhang ◽  
Min Xu ◽  
Qing Yang ◽  
Robert O. Ryan ◽  
Philip Howles ◽  
...  
Keyword(s):  
Independent Predictor ◽  
Dietary Lipids ◽  
Intestinal Lumen ◽  
Lymphatic Transport ◽  
Wild Type ◽  
Plasma Triglycerides ◽  
Apolipoprotein A ◽  
Threefold Increase ◽  
Postprandial Hypertriglyceridemia ◽  
Steady State Absorption

Apolipoprotein A-V (apoA-V), a liver-synthesized apolipoprotein discovered in 2001, strongly modulates fasting plasma triglycerides (TG). Little is reported on the effect of apoA-V on postprandial plasma TG, an independent predictor for atherosclerosis. Overexpressing apoA-V in mice suppresses postprandial TG, but mechanisms focus on increased lipolysis or clearance of remnant particles. Unknown is whether apoA-V suppresses the absorption of dietary lipids by the gut. This study examines how apoA-V deficiency affects the steady-state absorption and lymphatic transport of dietary lipids in chow-fed mice. Using apoA-V knockout (KO, n = 8) and wild-type (WT, n = 8) lymph fistula mice, we analyzed the uptake and lymphatic transport of lipids during a continuous infusion of an emulsion containing [3H]triolein and [14C]cholesterol. ApoA-V KO mice showed a twofold increase in3H ( P < 0.001) and a threefold increase in14C ( P < 0.001) transport into the lymph compared with WT. The increased lymphatic transport was accompanied by a twofold reduction ( P < 0.05) in mucosal3H, suggesting that apoA-V KO mice more rapidly secreted [3H]TG out of the mucosa into the lymph. ApoA-V KO mice also produced chylomicrons more rapidly than WT ( P < 0.05), as measured by the transit time of [14C]oleic acid from the intestinal lumen to lymph. Interestingly, apoA-V KO mice produced a steadily increasing number of chylomicron particles over time, as measured by lymphatic apoB output. The data suggest that apoA-V suppresses the production of chylomicrons, playing a previously unknown role in lipid metabolism that may contribute to the postprandial hypertriglyceridemia associated with apoA-V deficiency.

scholarly journals Use of NBD-cholesterol to identify a minor but NPC1L1-independent cholesterol absorption pathway in mouse intestine

2011 ◽  
Vol 300 (1) ◽  
pp. G164-G169 ◽  
Author(s):  
Michelle R. Adams ◽  
Eddy Konaniah ◽  
James G. Cash ◽  
David Y. Hui
Keyword(s):  
Intestinal Mucosa ◽  
Cholesterol Absorption ◽  
Intestinal Lumen ◽  
Cholesterol Transport ◽  
Cholesteryl Esters ◽  
Main Function ◽  
Absorption Mechanism ◽  
Ezetimibe Treatment ◽  
Niemann Pick ◽  
A Minor

The importance of Niemann-Pick C1 Like-1 (NPC1L1) protein in intestinal absorption of dietary sterols, including both cholesterol and phytosterols, is well documented. However, the exact mechanism by which NPC1L1 facilitates cholesterol transport remains controversial. This study administered 22-( N(-7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-23,24-bisnor-5-cholen-3β-ol (NBD-cholesterol) and [3H]cholesterol to Npc1l1+/+ and Npc1l1−/− mice to determine whether NPC1L1 facilitates dietary sterol uptake by enterocytes and/or participates in intracellular sterol delivery to the endoplasmic reticulum (ER) for lipoprotein assembly before secretion into plasma circulation. Results showed that [3H]cholesterol absorption was reduced but not abolished in Npc1l1−/− mice compared with Npc1l1+/+ mice. In the presence of Pluronic L-81 to block pre-chylomicron exit from the ER, significant amounts of [3H]cholesterol were found to be associated with lipid droplets in the intestinal mucosa of both Npc1l1+/+ and Npc1l1−/− mice, and the intracellular [3H]cholesterol can be esterified to cholesteryl esters. These results provided evidence indicating that the main function of NPC1L1 is to promote cholesterol uptake from the intestinal lumen but that it is not necessary for intracellular cholesterol transport to the ER. Surprisingly, NBD-cholesterol was taken up by intestinal mucosa, esterified to NBD-cholesteryl esters, and transported to plasma circulation to similar extent between Npc1l1+/+ and Npc1l1−/− mice. Ezetimibe treatment also had no impact on NBD-cholesterol absorption by Npc1l1+/+ mice. Thus, NBD-cholesterol absorption proceeds through an NPC1L1-independent and ezetimibe-insensitive sterol absorption mechanism. Taken together, these results indicate that NBD-cholesterol can be used to trace the alternative cholesterol absorption pathway but is not suitable for tracking NPC1L1-mediated cholesterol absorption.

scholarly journals The Roles of Dietary Glutamate in the Intestine

2018 ◽  
Vol 73 (Suppl. 5) ◽  
pp. 15-20 ◽  
Author(s):  
Daniel Tomé
Keyword(s):  
Monosodium Glutamate ◽  
Amino Acid Content ◽  
Intestinal Lumen ◽  
Free Form ◽  
Blood Levels ◽  
Umami Taste ◽  
Low Concentrations ◽  
Cephalic Phase ◽  
Gut Function ◽  
High Doses

Glutamate (Glu), either as one of the amino acids of protein or in free form, constitutes up to 8–10% of amino acid content in the human diet, with an intake of about 10–20 g/day in adults. In the intestine, postprandial luminal Glu concentrations can be of the order of mM and result in a high intra-mucosal Glu concentration. Glu absorbed from the intestinal lumen is for a large part metabolized by enterocytes in various pathways, including the production of energy to support intestinal motility and functions. Glu is the most important fuel for intestinal tissue, it is involved in gut protein metabolism and is the precursor of different important molecules produced within the intestinal mucosa (2-oxoglutarate, L-alanine, ornithine, arginine, proline, glutathione, γ-aminobutyric acid [GABA]). Studies in adult humans, pigs, piglets or preterm infants indicate that a large proportion of Glu is metabolized in the intestine, and that for the usual range of Glu dietary intake (bound Glu and free Glu including added Glu as a food additive in normal amounts up to 1 g/day), circulating Glu is tightly maintained at rather low concentrations. Systemic blood levels of Glu transiently rise when high doses monosodium glutamate (> 10–12 g), higher than normal human dietary consumption, are ingested and normalize within 2 h after the offset of consumption. Glu is also involved in oral and post oral nutrient chemosensing that involves gustatory nerves and both humoral and neural (vagal) gut-brain pathways with an impact on gut function and feeding behavior. Glu functions as a signaling molecule in the enteric nervous system and modulates neuroendocrine reflexes in the gastrointestinal tract. The oral taste sensation of Glu involves its binding to the oral umami taste receptors that triggers the cephalic phase response of digestion to prepare for food digestion. Glu is sensed again in the gut, inducing a visceral sensation that enhances additional gut digestive processes through the visceral sense (vago-vagal reflex).

Release of intestinal diamine oxidase by histamine in rats

1983 ◽  
Vol 61 (4) ◽  
pp. 349-355 ◽  
Author(s):  
Armin Wollin ◽  
Henri Navert
Keyword(s):  
Intestinal Mucosa ◽  
Oxidase Activity ◽  
Diamine Oxidase ◽  
Fold Increase ◽  
Lymph Flow ◽  
Intestinal Lumen ◽  
Enzyme Release ◽  
Storage Site ◽  
Diamine Oxidase Activity ◽  
Dose Dependent

Diamine oxidase activity was measured in the intestinal mucosa, lymph, and in the serum of rats, to determine whether histamine, a substrate of diamine oxidase, liberates this enzyme from its mucosal storage site(s). Histamine induced a sharp rise in intestinal lymph flow, lymph protein, and lymph diamine oxidase, lasting less than 1 h after the histamine injection. The rise in lymph diamine oxidase activity was dose dependent over a narrow concentration range (0.05–0.2 mmol/kg, i.v. and 0.15–0.6 mmol/kg i.d.). It did not correlate with the dose dependent increase in lymph flow or lymph protein. A single maximal intraduodenal dose of histamine caused a 41.6-fold increase in the lymph diamine oxidase activity and a 2.4-fold increase in the serum enzyme level temporarily. A second injection of histamine, 2 h after the first, resulted in a comparatively smaller increase in the lymph enzyme. The extent of the reduction was dependent on the magnitude of the first injection. The results suggest that histamine causes a limited liberation of diamine oxidase from the intestinal mucosa. The function of this enzyme release may be a protective response by the mucosa to reduce toxic levels of free histamine, either liberated by the mucosal tissue or absorbed from the intestinal lumen.

scholarly journals Determinants of hypoxia-inducible factor activity in the intestinal mucosa

2017 ◽  
Vol 123 (5) ◽  
pp. 1328-1334 ◽  
Author(s):  
Raphael R. Fagundes ◽  
Cormac T. Taylor
Keyword(s):  
Intestinal Mucosa ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Hypoxia Inducible Factor ◽  
Oxygen Demand ◽  
Intestinal Lumen ◽  
Adaptation To Hypoxia ◽  
Healthy Mucosa ◽  
Microenvironmental Factors ◽  
Anoxic Environment

The intestinal mucosa is exposed to fluctuations in oxygen levels due to constantly changing rates of oxygen demand and supply and its juxtaposition with the anoxic environment of the intestinal lumen. This frequently results in a state of hypoxia in the healthy mucosa even in the physiologic state. Furthermore, pathophysiologic hypoxia (which is more severe and extensive) is associated with chronic inflammatory diseases including inflammatory bowel disease (IBD). The hypoxia-inducible factor (HIF), a ubiquitously expressed regulator of cellular adaptation to hypoxia, is central to both the adaptive and the inflammatory responses of cells of the intestinal mucosa in IBD patients. In this review, we discuss the microenvironmental factors which influence the level of HIF activity in healthy and inflamed intestinal mucosae and the consequences that increased HIF activity has for tissue function and disease progression.

Nutrients regulate diamine oxidase release from intestinal mucosa

1998 ◽  
Vol 275 (4) ◽  
pp. R969-R975 ◽  
Author(s):  
Armin Wollin ◽  
Xiaolin Wang ◽  
Patrick Tso
Keyword(s):  
Intestinal Mucosa ◽  
Oxidase Activity ◽  
Diamine Oxidase ◽  
Lipid Absorption ◽  
Intestinal Lumen ◽  
Enzyme Release ◽  
Distal Small Intestine ◽  
Intestinal Lymph ◽  
Diamine Oxidase Activity ◽  
Chylomicron Formation

Diamine oxidase is continuously released from the intestinal mucosa and carried to the circulation by the lymphatics. The effect of nutrients on this release was examined. Rats were prepared with duodenal and intestinal lymph cannulas. Test mixtures of lipid emulsions containing triolein, oleic acid, or tricaprylin and solutions of carbohydrate and protein were infused into the duodenum. The enzyme release and triglyceride transport were determined and in some experiments were done in the presence and absence of Pluronic L-81, an inhibitor of chylomicron formation, and aminoguanidine, an inhibitor of diamine oxidase activity. The data indicate that nonlipid nutrients did not increase diamine oxidase activity in the intestinal lymph, but the mucosal tissue content was significantly reduced in the distal small intestine, particularly after protein infusion. Triglycerides and fatty acids increased diamine oxidase in the intestinal lymph, and the longer-chain triglyceride was more effective. Inhibition of triglyceride transport did not interfere with the enzyme release, and the inhibition of diamine oxidase activity had no significant effect on lipid absorption. According to our observations, only lipids increase intestinal lymph diamine oxidase. Nonfat nutrients appear to increase diamine oxidase in the intestinal lumen. Diamine oxidase is not directly required for lipid absorption.

Ultrastructural effects of intravascularly injected polyethylene glycol-hemoglobin in intestinal mucosa

1998 ◽  
Vol 275 (2) ◽  
pp. H615-H625 ◽  
Author(s):  
Ann L. Baldwin ◽  
Lisa M. Wilson ◽  
J. Edward Valeski
Keyword(s):  
Mast Cell ◽  
Polyethylene Glycol ◽  
Intestinal Mucosa ◽  
Time Course ◽  
Mast Cell Degranulation ◽  
Intestinal Lumen ◽  
Saline Control ◽  
Mucosal Mast Cell ◽  
Sprague Dawley ◽  
Cell Secretion

Polyethylene glycol (PEG)-conjugated Hb (PEG-Hb) is being considered as a blood substitute. Previously, we showed that PEG-Hb extravasates rapidly from the intestinal mucosa and causes transient epithelial sloughing, resulting in temporary unimpeded passage of material between the intestinal lumen and the microcirculation. The present study quantifies the time course of factors related to this disturbance. Anesthetized Sprague-Dawley rats (350–450 g) were injected with a bolus of PEG-Hb (10 mg/ml) in saline. Control animals received saline, alone or with Dextran 70 (5 mg/ml). After 2, 8, 15, 60, or 90 min, the small intestine was perfusion fixed for microscopy (4 animals for each time point). Epithelial cell detachment and mucosal mast cell degranulation peaked at 2 and 8–15 min, respectively, but by 90 min were back to normal. Goblet cell secretion increased with time up to 8–15 min, after which it leveled off. Mean interstitial width was significantly greater 8 min after injection than for controls and continued to increase with time. In capillaries, endothelial fenestral diaphragms were replaced by thick, amorphous structures. Mesenteric mast cell degranulation was significantly greater 60–90 min after injection compared with controls. We propose that these results are consistent with intravascular injection of PEG-Hb invoking a transient inflammatory response in the intestine.

scholarly journals Is apolipoprotein A-IV rate limiting in the intestinal transport and absorption of triglyceride?

2013 ◽  
Vol 304 (12) ◽  
pp. G1128-G1135 ◽  
Author(s):  
Alison B. Kohan ◽  
Fei Wang ◽  
Xiaoming Li ◽  
Abbey E. Vandersall ◽  
Sarah Huesman ◽  
...  
Keyword(s):  
Intestinal Mucosa ◽  
Dietary Fat ◽  
Intestinal Transport ◽  
Dietary Lipid ◽  
Lipid Absorption ◽  
Lymphatic Transport ◽  
Apolipoprotein A ◽  
Rate Limiting

Apolipoprotein A-IV (apoA-IV) is synthesized by the intestine and secreted when dietary fat is absorbed and transported into lymph associated with chylomicrons. We have recently demonstrated that loss of apoA-IV increases chylomicron size and delays its clearance from the blood. There is still uncertainty, however, about the precise role of apoA-IV on the transport of dietary fat from the intestine into the lymph. ApoA-IV knockout (KO) mice do not have a gross defect in dietary lipid absorption, as measured by oral fat tolerance and fecal fat measurements. Here, using the in vivo lymph fistula mouse model, we show that the cumulative secretion of triglyceride (TG) into lymph in apoA-IV KO mice is very similar to that of wild-type (WT) mice. However, the apoA-IV KO mice do have subtle changes in TG accumulation in the intestinal mucosa during a 6-h continuous, but not bolus, infusion of lipid. There are no changes in the ratio of esterified to free fatty acids in the intestinal mucosa of the apoA-IV KO, however. When we extended these findings, by giving a higher dose of lipid (6 μmol/h) and for a longer infusion period (8 h), we found no effect of apoA-IV KO on intestinal TG absorption. This higher lipid infusion most certainly stresses the intestine, as we see a drastically lower absorption of TG (in both WT and KO mice); however, the loss of A-IV does not exacerbate this effect. This supports our hypothesis that apoA-IV is not required for TG absorption in the intestine. Our data suggest that the mechanisms by which the apoA-IV KO intestine responds to intestinal lipid may not be different from their WT counterparts. We conclude that apoA-IV is not required for normal lymphatic transport of TG.

Sign in / Sign up

Export Citation Format

Share Document