Role of phospholipids in lymphatic transport of dietary lipids in the dog

1960 ◽  
Vol 199 (6) ◽  
pp. 1015-1020 ◽  
Author(s):  
Alfred J. Rampone

The phospholipids of lymph have been measured in relation to the total lipid in 16 chronic thoracic duct fistula dogs during the postabsorptive state and following the administration of various lipid types in the diet. It was found that phospholipid transport related linearly to total lipid transport under all conditions studied, including the postabsorptive state. The percentage of lymph lipid transported as phospholipid ranged from 3 to 18% and was independent of the type of lipid fed. Depriving the animals of phospholipid precursors in the diet for as long as 90 days previously failed to alter this relationship or the total quantity of lipid transported. The total quantity of phospholipid which could be considered as having been newly synthesized as a direct result of processes underlying absorption of exogenous (dietary) fats was small and probably insignificant. The conclusion is reached that phospholipids probably do not serve as intermediates in the absorptive process, nor do they constitute important vehicles for fatty acid transport in lymph.

2007 ◽  
Vol 293 (5) ◽  
pp. E1207-E1214 ◽  
Author(s):  
J. Patrick Kampf ◽  
Danielle Parmley ◽  
Alan M. Kleinfeld

The role of cell membranes in regulating the flux of long chain free fatty acids (FFA) into and out of adipocytes is intensely debated. Four different membrane proteins including, FABPpm, CD36/FAT, caveolin-1, and FATP have been identified as facilitating FFA transport. Moreover, CD36 and caveolin-1 are also reported to mediate transport in conjunction with lipid rafts. The principal evidence for these findings is a correlation of the level of FFA uptake with the expression level of these proteins and with the integrity of lipid rafts. The 3T3-L1 and 3T3-F442A cell lines in their preadipocyte states reveal little or no expression of these proteins and correspondingly low levels of uptake. Here we have microinjected the adipocyte and preadipocyte cell lines with ADIFAB, the fluorescent indicator of FFA. The ADIFAB fluorescence allowed us to monitor the intracellular unbound FFA concentration during FFA influx and efflux. We show that these measurements of transport, in contrast to FFA uptake measurements, correlate neither with expression of these proteins nor with lipid raft integrity in preadipocytes and adipocytes. Transport characteristics, including the generation of an ATP-dependent FFA concentration gradient, are virtually identical in adipocytes and preadipocytes. We suggest that the origin of the discrepancy between uptake and our measurements is that most of the FFA transported into the cells is lost during the uptake but not in the transport protocols. We conclude that long chain fatty acid transport in adipocytes is very likely mediated by an as-yet-unidentified membrane protein pump.


2012 ◽  
Vol 303 (7) ◽  
pp. E899-E907 ◽  
Author(s):  
M. A. Poreba ◽  
C. X. Dong ◽  
S. K. Li ◽  
A. Stahl ◽  
J. H. Miner ◽  
...  

The antidiabetic intestinal L cell hormone glucagon-like peptide-1 (GLP-1) enhances glucose-dependent insulin secretion and inhibits gastric emptying. GLP-1 secretion is stimulated by luminal oleic acid (OA), which crosses the cell membrane by an unknown mechanism. We hypothesized that L cell fatty acid transport proteins (FATPs) are essential for OA-induced GLP-1 release. Therefore, the murine GLUTag L cell model was used for immunoblotting, [3H]OA uptake assay, and GLP-1 secretion assay as determined by radioimmunoassay following treatment with OA ± phloretin, sulfo- N-succinimidyl oleate, or siRNA against FATP4. FATP4−/− and cluster-of-differentiation 36 (CD36)−/− mice received intraileal OA, and plasma GLP-1 was measured by sandwich immunoassay. GLUTag cells were found to express CD36, FATP1, FATP3, and FATP4. The cells demonstrated specific 3H[OA] uptake that was dose-dependently inhibited by 500 and 1,000 μM unlabeled OA ( P < 0.001). Cell viability was not altered by treatment with OA. Phloretin and sulfo- N-succinimidyl oleate, inhibitors of protein-mediated transport and CD36, respectively, also decreased [3H]OA uptake, as did knockdown of FATP4 by siRNA transfection ( P < 0.05–0.001). OA dose-dependently increased GLP-1 secretion at 500 and 1,000 μM ( P < 0.001), whereas phloretin, sulfo- N-succinimidyl oleate, and FATP4 knockdown decreased this response ( P < 0.05–0.01). FATP4−/− mice displayed lower plasma GLP-1 at 60 min in response to intraileal OA ( P < 0.05), whereas, unexpectedly, CD36−/− mice displayed higher basal GLP-1 levels ( P < 0.01) but a normal response to intraileal OA. Together, these findings demonstrate a key role for FATP4 in OA-induced GLP-1 secretion from the murine L cell in vitro and in vivo, whereas the precise role of CD36 remains unclear.


1958 ◽  
Vol 37 (10) ◽  
pp. 1333-1341 ◽  
Author(s):  
Donald S. Fredrickson ◽  
Duncan L. McCollester ◽  
Katsuto Ono

Physiology ◽  
2013 ◽  
Vol 28 (2) ◽  
pp. 125-134 ◽  
Author(s):  
Carolina Hagberg ◽  
Annika Mehlem ◽  
Annelie Falkevall ◽  
Lars Muhl ◽  
Ulf Eriksson

Dietary lipids present in the circulation have to be transported through the vascular endothelium to be utilized by tissue cells, a vital mechanism that is still poorly understood. Vascular endothelial growth factor B (VEGF-B) regulates this process by controlling the expression of endothelial fatty acid transporter proteins (FATPs). Here, we summarize research on the role of the vascular endothelium in nutrient transport, with emphasis on VEGF-B signaling.


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