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INTRODUCTION |
The similarities in lipid fatty acid composition of lymph and bile and the involvement of biliary phospholipids in the formation of interprandial intestinal lipoproteins have been noted by several authors (Baxter 1966
, Boucrot and Clément 1969, Karmen et al. 1963, Ockner et al. 1969, Shiau et al. 1985, Shrivastava et al. 1967, Whyte et al. 1963). In the postprandial state, the triglyceride fatty acid composition of chylomicrons greatly resembles the lipid fed to the subject (Feldman et al. 1983). The fatty acid composition of chylomicron phospholipids is influenced by the dietary fatty acids to a much smaller extent because biliary phosphatidylcholine is used to a greater extent than dietary phosphatidylcholine in supplying phosphatidylcholine for the chylomicron surface coat (Mansbach 1977, Patton et al. 1984, Whyte et al. 1963). On the other hand, long-term diets have been shown to affect the fatty acid composition of biliary phospholipids (Herzberg et al. 1992, Levy and Herzberg 1995). Moreover, we have demonstrated that biliary phospholipid output can be affected by the prefed diet in unfed animals. Indeed, biliary phospholipid output was 37-59% lower in rats prefed a high medium-chain triglyceride oil diet (HMCT)3 than in rats prefed a high sunflower oil diet (HSFO), a high menhaden oil diet (HMO) or a low-fat diet (LF) (Degrace et al. 1998). In this early study, the composition of plasma fatty acids was altered by the prefed diet, and plasma fatty acid contribution to intestinal lipoprotein formation was evoked.
In the postprandial state, both blood and bile flows are thought to be increased (Baxter 1966, Coleman and Rahman 1992, Gangl and Ockner 1975, Karmen et al. 1963, Whyte et al. 1963). Consequently, after a single fat meal, exogenous fatty acids mix with endogenous fatty acids in the enterocyte and both contribute to the constitution of the intestinal lymph lipoprotein (Herzberg et al. 1992, Ockner et al. 1969, Shiau et al. 1985, Tso and Scobey 1986).
In this study, we have tried to establish whether the observed alteration of endogenous fatty acids by long-term lipid diets could modify the absorption process of a single fatty meal. Rats were prefed either a low-fat diet (3.5 g/100 g) or different high-fat diets containing sunflower oil, menhaden oil or medium-chain triglyceride oil (15 g/100 g), then given intraduodenally a 90-µmol lipid emulsion containing [3H] oleic acid (OA) and [14C] arachidonic acid (AA). The level of these two labeled fatty acids recovered in the lymph and the fatty acid composition and output in the lymph were recorded.
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MATERIALS AND METHODS |
Animals.
Official French regulations for the care and use of laboratory animals were followed throughout. Male Wistar rats weighing 173.6 ± 3.5 g were obtained from Centre d'élevage Dépré (Saint Doulchard, France). Before the initiation of the study, rats were housed for 1 wk in a controlled environment, with constant temperature and humidity and a dark period from 2000 to 0800 h. They were fed a standard nonpurified diet containing the following (g/100 g): lipid, 3.5; carbohydrate, 67; protein, 19.4; cellulose, 4.5; and minerals, 5.7 (AO4, UAR Epinay sur Orge, France). They had free access to tap water.
Rats were divided into groups and fed either low-fat (3.5 g/100 g) or high-fat (15 g/100 g) diets. High-fat diets were prepared by adding sunflower, menhaden or medium-chain triglyceride oil to a lipid-free powder containing the following (g/100 g): carbohydrate, 63.5; protein, 22.5; cellulose, 6; and minerals, 7 (UAR). The rats were fed for 4 wk. Sunflower oil was purchased at a local store, menhaden oil was donated by the Zapata Protein Society (Reedville, VA) and medium-chain triglyceride oil (CERES-MCT) by Astra Calvé-Unilever (Paris la Défense, France).
Surgical procedures.
A mesenteric lymph duct cannulation was performed on fed rats of each diet group, with the use of a heparinized polyethylene catheter (i.d. 0.3 mm, o.d. 0.7 mm, Biotrol, Paris, France) (Bollman et al. 1948). For lipid infusion, a second catheter (i.d. 0.76 mm, o.d. 1.22 mm, Biotrol) was inserted in the duodenum in a caudal direction and fixed in a manner that allowed the circulation of luminal contents. The cannulae were exteriorized through incisions in the flanks. Immediately after surgery, rats were placed in restraining cages in an air-conditioned room (25°C). They did not receive any solid food but had free access to a water solution containing sodium chloride (7 g/L) and potassium chloride (2 g/L). Quantities consumed were controlled and estimated to be largely sufficient to replenish the fluid and electrolyte losses due to lymphatic drainage.
Lymph collection.
The morning after surgery, lymph of starved rats was collected for 3 h (lymph 0 h) in tubes moistened with a solution of ethylenediaminetetraacetic acid (268 mmol/L) and placed inside Dewar flasks containing ice. A 90-µmol lipid emulsion was infused as a single dose through the duodenal catheter and the lymph was collected for 3 h (lymph 0-3 h). The lymph samples were immediately analyzed for phospholipid, triglyceride and fatty acid concentration. Rats were discarded if the lymph flow was <1 mL/h in the starved state and if it had not increased two- to threefold during lipid absorption .
Lipid mixtures.
The lipid emulsion was composed of 25 µmol linoleic acid (LA), 5 µmol AA, 30 µmol OA and 30 µmol monopalmitin (PA). [3H] OA [9,10-3H] OA; 672 kBq; specific activity, 370 GBq/mmol) and [1-14C] AA (100 kBq; specific activity, 2.03 GBq/mmol) were added to the emulsion.
For the preparation, lipids were dissolved in ether; after evaporation, 1.5 mL of physiological serum containing 60 µmol sodium taurocholate was added. Lipid molecules were purchased from Nu-Chek-Prep (Elysian, MN) or Sigma (Saint Quentin-Fallavier, France). The labeled fatty acids were obtained from CEA (Gif sur Yvette, Saclay, France). Sodium taurocholate was purchased from Sigma.
Fatty acid analysis.
Lipid extraction was carried out on the remainder of the infused lipid emulsion, on aliquots from intestinal lymph, on the intestinal mucosa and on the contents of the small intestine. Lipids were extracted with dimethoxymethane/methanol (4:1, v/v) (Delsal 1944), dried with absolute ethanol and dissolved in chloroform.
Lymph lipid fatty acids were methylated in the presence of boron trifluoride (Slover and Lanza 1979) with heptadecanoic acid as the internal standard. Methyl esters were extracted by using hexane and separated by gas/liquid chromatography (GLC). These studies were conducted on a Chrompack (Les Ulis, France) chromatograph and column (CP Wax 52CB 50 m) with helium carrier gas. The initial temperature was 55°C, increasing to 235°C via a program controlling temperature. The fatty acids were identified by comparison of retention times with known standards from Nu-Chek-Prep. The peak areas were measured by a Chromjet integrator (Spectra-Physics, San Jose, CA), which automatically calculates fatty acid percentages and amounts.
Thin layer chromatography was conducted on 500-µm silica gel by using a hexane/ether/methanol/acetic acid (90:20:3:2, v/v/v/v) solvent system (Stahl et al. 1956) to separate different lipid fractions. Bands were scraped from the plates; after elution with methanol, the radioactivity of the different fractions was measured.
The radioactivity of the total lipid extracts from the remainder of the infused lipid emulsion, lymph samples, intestinal mucosa and contents of the small intestine and of the different lipid fractions obtained by thin layer chromatography was determined using a Packard Prias PLD Tricarb liquid scintillation spectrophotometer (Packard Instruments, Downers Grove, IL) after Permafluor III (Packard Instruments) diluted with xylene (1:9, v/v) was added to the samples.
Calculations.
The percentage of radioactivity administered in the intestinal lumen recovered in the lymph was calculated as follows: 100(radioactivity in the lymph)/(radioactivity in the lipid emulsion infused 
radioactivity in the rest of the emulsion).
Lymphatic lipid fatty acid output was assessed by both radioactivity and GLC determinations. Radioactive OA and AA output reflects the transport of exogenous fat into the lymph, whereas the GLC method determines the transport of both exogenous and endogenous lipid fatty acids into the lymph. Thus the endogenous fatty acid contribution to lymph lipid was calculated by subtracting the exogenous value from the total (exogenous and endogenous) value.
Differences in mean values among diet groups were tested by one-way ANOVA or by two-way ANOVA when factors were time and diet. Significant differences between means were tested by Student's t test for an independent variable (Snedecor and Cochran 1967). When variances and number of rats were unequal, means were tested by a nonparametric test (Siegel 1956).
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RESULTS |
Weight gains were not significantly different among rats fed the various diets for 4 wk (+105 ± 5 g for LF, +102.2 ± 4.8 g for HSFO, +96.7 ± 3.8 g for HMO and +83.9 ± 15.4 g for HMCT).
The OA and AA lymph absorption profiles (Fig. 1) showed that the absorption peak for rats prefed the LF, HMO and HMCT diets occurred within 1 h. From 72 to 95% of the total radioactivity recovered in the 6 h was recovered in the first 3 h. Consequently, for lymphatic absorption studies, lymph was collected for 3 h after intestinal infusion of the lipid emulsion containing the two labeled fatty acids.
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| Fig 1.
Lymphatic [3H] oleic acid (OA) and [14C] arachidonic acid (AA) recoveries as a percentage of radioactive lymphatic lipid output in rats prefed a low-fat diet (LF), a menhaden oil (HMO) or a medium-chain triglyceride (HMCT) diet for 4 wk. Lymph was collected every 30 min or every hour during the 6 h after the luminal infusion of the lipid emulsion. Radioactive [3H]oleic acid (OA) and [14C] arachidonic acid (AA) recoveries in mesenteric lymph were expressed as a percentage of total output (6 h). Values are means ± SEM, n = 3.
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Because the HSFO diet has a fatty acid composition that is not different than that of the LF diet (Table 1), any changes observed in the lymph studies of rats prefed the HSFO diet rather than the LF diet were due only to the difference in the lipid quantity administered.
Lymph fatty acid composition and output.
For rats prefed the LF, HSFO and HMO diets, the total fatty acid output was significantly greater in the lymph collected during the 3 h after the infusion of the lipid emulsion than in the lymph of starved rats (0 h), whereas it was unaffected by infusion in rats prefed HMCT (Fig. 2). The total lymph fatty acid output was significantly greater for rats prefed the HSFO and the HMO diets than for those fed the LF and HMCT diets.
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| Fig 2.
Total lymph fatty acid output before and after the infusion of the lipid emulsion in rats prefed a low-fat diet (LF), a high sunflower oil (HSFO), a menhaden oil (HMO) or a medium-chain triglyceride (HMCT) diet for 4 wk. Lymph was collected as described in Materials and Methods for 3 h before (lymph 0 h) and for 3 h after the infusion of the lipid emulsion (lymph 0-3 h). Results are means ± SEM, n = 4-8 as in Table 3. Values assigned different letters are significantly different, P < 0.05. *P < 0.05 and  P < 0.001, significantly different than lymph 0 h.
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Whatever the long-chain fatty acid prefed diet, the fatty acid composition of the lymph collected from 0 to 3 h after lipid infusion (Table 2) suggested a dilution of lipid emulsion exogenous fatty acids by endogenous fatty acids. Indeed, the emulsion fatty acid ratio (PA/OA/LA/AA = 10:12:10:2) was never conserved in the lymph collected from 0 to 3 h after lipid infusion (LF, 10:8:12:3; HSFO, 10:9:22:4; HMO, 10:6:3:1; HMCT, 10:9:6:3). Whatever the prefed diet, some fatty acids that were not present in the emulsion were increased in the lymph collected from 0 to 3 h after lipid infusion, for example, 22:6(n-3) in rats prefed HMO.
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Table 2.
Fatty acid composition of the emulsion and of intestinal lymph before and after the infusion of the emulsion in rats prefed low-fat (LF), sunflower oil high-fat (HSFO), menhaden oil high-fat (HMO) or medium-chain triglyceride oil high-fat (HMCT) diets1
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As expected, the lymph outputs (µmol/3 h) of fatty acids that constituted the emulsion infused were increased (Table 3). In rats prefed the LF diet, 18:1(n-9) was the fatty acid that increased to the greatest extent, whereas 16:0 and 20:4(n-6) in rats prefed HSFO, and 16:0 and 18:1(n-9) in rats prefed HMO increased the most. On the other hand, in rats prefed HMCT, among the four fatty acids constituting the emulsion, only 18:2(n-6) was significantly increased in the lymph collected from 0 to 3 h after lipid infusion.
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Table 3.
Fatty acid amounts in the emulsion and fatty acid output in the lymph before and after the infusion of the emulsion in rats prefed low-fat (LF), sunflower oil high-fat (HSFO), menhaden oil high-fat (HMO) or medium-chain triglyceride oil high-fat (HMCT) diets1
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Mesenteric lymph recovery of the two labeled exogenous fatty acids.
During the 3 h after intestinal infusion, the presence of exogenous [3H] OA was significantly greater than that of the [14C] AA in the lymph of rats prefed both the LF and HSFO diets (Table 4). However, the percentage of recovery of [3H] OA was significantly higher in the mesenteric lymph of rats prefed the HSFO diet than in those prefed the LF diet.
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Table 4.
Percentage of luminally administered radioactivity recovered in the lymph in rats prefed low-fat (LF), sunflower oil high-fat (HSFO), menhaden oil high-fat (HMO) or medium-chain triglyceride oil high-fat (HMCT) diets1
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In rats prefed the HSFO, HMO or HMCT diet, the amount of labeled [3H] OA recovered in the mesenteric lymph during the 3 h after the duodenal infusion was highest in rats prefed HSFO and lowest in those prefed HMCT. Indeed, in rats prefed HMCT, the [3H] OA lymph recovery was 49.2% lower than in those prefed HSFO.
The lymph recovery of [14C] AA was also significantly lower in the lymph of rats prefed HMCT than in the lymph of those prefed HSFO and HMO.
Incorporation of exogenous 3H OA and 14C AA into lymph triglycerides and phospholipids.
Whatever the diet, the exogenous [3H] OA and [14C] AA were preferentially incorporated into triglycerides (Table 5). However, in rats prefed the LF diet exclusively, significantly less [14C] AA was incorporated into triglycerides than [3H] OA.
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Table 5.
Percentage of [3H] oleic and [14C] arachidonic acids recovered in lymph triglycerides and phospholipids in rats prefed low-fat (LF), sunflower oil high-fat (HSFO), menhaden oil high-fat (HMO) or medium chain triglyceride oil high-fat (HMCT) diets1
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The incorporation of the two labeled fatty acids into phospholipids was significantly higher for the [14C] AA than for the [3H] OA in all groups except rats prefed HMCT. Although the percentage of [3H] OA incorporated into phospholipids was not significantly different whatever the prefed diet, the HSFO diet was responsible for a lower incorporation of [14C] AA into the lymph phospholipids compared with the LF diet, and the [14C] AA incorporation into phospholipids was higher in rats prefed HMO than in those prefed HSFO or HMCT. The lymph [3H] OA triglyceride/phospholipid ratio was lower in all rats prefed a high-fat diet than in those prefed the LF diet, whereas it was greater for [14C] AA in rats prefed HSFO and HMCT than in those prefed LF and HMO.
Lymph endogenous OA and AA content.
In the starved rats, lymph lipid fatty acids are of endogenous origin. After the infusion of the lipid emulsion, lymph endogenous OA or AA content, compared with that of starved rats, was increased in rats prefed long-chain fatty acid diets (LF, HSFO and HMO) (Table 6).
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Table 6.
Lymph endogenous oleic and arachidonic acid contents in rats prefed low-fat (LF), sunflower oil high-fat (HSFO), menhaden oil high-fat (HMO) or medium chain triglyceride oil high-fat (HMCT) diets1
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On the other hand, in rats prefed HMCT, the infusion of the lipid emulsion did not lead to an increase of endogenous OA or AA levels in the lymph compared with the outputs in lymph of starved rats. Moreover, endogenous AA content in the lymph of rats prefed HMCT collected after the infusion of lipid emulsion was significantly lower than that in the lymph of the rats prefed the other three diets.
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DISCUSSION |
In this study, we investigated intestinal lymph absorption of fatty acids from a lipid emulsion in rats prefed different fat diets for 4 wk, a time period over which fatty acid changes can become stabilized in the organism. In this investigation, we clearly demonstrate an effect of diet on lymph fatty acid output in the postprandial state.
As expected, in rats prefed the long-chain fatty acid diets, the total lymph fatty acid output increased during the 3 h after the infusion of the lipid emulsion in comparison with the lymph total fatty acid output of starved rats. On the other hand, in rats prefed HMCT, the infusion of the same lipid emulsion did not increase the total lymph fatty acid output. Results concerning the intestinal lymph absorption of the emulsion administered to rats prefed HMCT must be interpreted in the light of the results obtained in our previous report discussing the characteristics of plasma and bile lipids (Degrace et al., 1998).
Prefeeding an HSFO or HMO diet led to 32 and 65% greater total lymph fatty acid output, respectively, compared with rats prefed LF. These results are in agreement with those of Mansbach and Arnold (1986) who showed a 60% greater triglyceride output in the lymph in rats prefed fat compared with controls fed nonpurified diets. Such results were also obtained for [3H] OA in rats prefed HSFO and for [14C] AA in rats prefed the HMO diet vs. those prefed the LF diet.
The results provided further evidence that a dilution of exogenous fatty acids from the emulsion by endogenous fatty acids occurred, clearly demonstrating that this dilution was modified according to the fatty acid studied and to the nature of the prefed diet. In rats prefed LF, 12.45 µmol of OA (41.5% of the 30 µmol of [3H] OA administered) and 1.53 µmol of AA (30.6% of the 5 µmol of [14C] AA administered) should have been recovered in the lymph collected from 0 to 3 h after lipid infusion. However, the values recorded in Table 3 were much higher (20.8 and 7.8 µmol/3 h, respectively). In rats prefed HSFO or HMO, 16.4 or 13.4 µmol of OA and 2.03 or 2.16 µmol of AA should have been recovered in the lymph collected from 0 to 3 h after lipid infusion, whereas 18.5 or 26.0 and 11.1 or 5.9 µmol/3 h, respectively, were actually obtained.
This dilution of exogenous fatty acids by endogenous fatty acids was undoubtedly due to an intervention of biliary phospholipids as suggested by their fatty acid composition and the increases of 16:0 and 20:4(n-6) levels in the lymph of rats prefed HSFO and of 16:0 and 18:1(n-9) in the lymph of those prefed HMO. The biliary phospholipid output augmentation occurring after a fat meal was reported to be greater in rats prefed high-fat rather than low-fat diets (Knox et al. 1991) and could be explained as follows: High long-chain fatty acids loads had a maximum trophic effect in the mid-area of the small intestine (Jenkins and Thompson 1993) and could increase the capacity of this area to absorb fat. Indeed, when the lipid emulsion was infused, the constituent lipids were absorbed in the proximal small intestine and did not impair the absorption of bile acids coming from the bile and the emulsion taurocholate (Schiff et al. 1972), which were able to stimulate biliary phospholipid production (Cohen et al. 1990, Young and Hanson 1972, Yousef and Fischer 1976).
Fatty acids such as 16:1(n-7), 20:5(n-3) and 22:6(n-3), which were not present in the emulsion but whose appearance in the bile and plasma lipids after the 4-wk HMO diet was demonstrated in our previous study (Degrace et al., 1998), were increased in the lymph collected from 0 to 3 h after lipid infusion. For example, the output of 20:5(n-3) obtained in the bile of starved rats was 1.0 µmol/3 h. If bile phospholipids are considered to be the only suppliers of endogenous fatty acids in the postprandial state, this means that the output of 20:5(n-3) has increased 15-fold to supply the 15.8 µmol found in the lymph collected from 0 to 3 h after lipid infusion. Because such an increase was not obtained for fatty acids of the emulsion, endogenous fatty acids from sources other than bile may have contributed to the formation of intestinal lipoproteins. Under normal conditions, endogenous acyl groups entering the enterocyte as fatty acids from the plasma are not ultimately transported in the lymph (Gangl and Ockner 1975) but are destined for the most part to serve the structural and energy requirements of the epithelium itself. In this particular case [an (n-3) fatty acid-rich prefed diet], the substantial lymph (n-3) fatty acid output could be explained by an increased production of biliary phospholipids or by the presence of (n-3) fatty acids coming from plasma in response to the low levels of 18:2(n-6) and the high levels of (n-3) fatty acid in adipose tissue, plasma, bile and liver (Degrace et al. 1998).
Although OA and AA were preferentially incorporated into lymphatic triglycerides, AA was incorporated to a larger extent than OA into phospholipids, in accordance with several reports (Carlier et al. 1991, Chen et al. 1985, Mathieu et al. 1996, Nilsson et al. 1987, Pavero et al. 1992). A higher incorporation of exogenous [14C] AA into the lymph phospholipids of HMO relative to rats prefed HSFO was observed; this suggests that a higher contribution of exogenous AA to lymph phospholipid formation occurred in response to the low biliary AA concentration. As a matter of fact, under normal feeding conditions, biliary phosphatidylcholine is the main supplier of lymph phospholipids (Tso and Scobey 1986, Whyte et al. 1963).
In contrast to observations concerning the rats prefed the other high-fat diets, the total lymph fatty acid output of rats prefed HMCT was not increased during the 3 h after the infusion of the emulsion, despite a lymphatic absorption of the two labeled fatty acids reaching 27% for [3H] OA and 21% for [14C] AA. In this case, only the fatty acids largely represented in the emulsion were increased in the lymph collected from 0 to 3 h after lipid infusion, suggesting a low dilution of exogenous fatty acids by endogenous fatty acids. This hypothesis is consistent with the low biliary phospholipid output observed in this group of rats before food consumption (Degrace et al. 1998) and was confirmed by the absence of any increase in endogenous OA and AA lymph levels (Table 6). Studies focusing on biliary flow and phospholipid output in rats prefed HMCT after a fat meal are very scarce; however, Shinohara et al. (1993) found that total bile acids in the upper jejunum were 50% lower in rats fed a high MCT diet relative to those fed a high long-chain triglyceride diet and concluded that MCT feeding likely decreases secretion of bile into the lumen.
During the 4-wk period of the HMCT diet consumption, although lymphatic absorption due to the presence of monoglycerides took place, fatty acids were absorbed rapidly via the portal vein (Greenberger et al. 1966, Tso et al. 1995, Vallot et al. 1985) as a result of the early action of preduodenal and pancreatic lipases. Such a diet has been shown to result in greater mucosa and cell proliferation, with maximal effects in the proximal small intestine (Jenkins and Thompson 1993). In the HMCT diet group, a longer portion of intestine is needed to allow uptake and absorption of long-chain fatty acids of the emulsion into the lymph. This situation could impair the reabsorption of bile acids and subsequently the biliary phospholipid production, which was already low (Degrace et al. 1998). Moreover, the low levels of biliary phospholipids previously observed could accentuate the more distal absorption of emulsion lipids, as noted by Mansbach et al. (1985), who found lipids to be more proximately absorbed in the intestine when phosphatidylcholine was included in the infusate. It should be noted that the lymph fatty acid output obtained in 6 h after the infusion of the emulsion was less than the value obtained with starved rats (data not shown). This could correspond to a reduced biliary phospholipid production, occurring during the exogenous lipid absorption and resulting from the impairement of bile acid absorption in the distal intestine by the presence of lipids (Schiff et al. 1972).
Whatever the prefed diet, the radioactivity infused and the radioactivity remaining in the mucosa and the lumen at the end of the experiment remained the same. The 21-55% recoveries suggested that some of the [3H] OA and [14C] AA was transported either by noncannulated lymphatics and/or by a system other than the lymphatic system. Long-chain fatty acids, whatever their degree of saturation, are preferentially absorbed by the lymphatic pathway. Nevertheless, results obtained in this study with 20:4(n-6) confirmed that polyunsaturated fatty acids are recovered less in the lymph than OA (Bernard and Carlier 1991, Carlier et al. 1991, MacDonald et al. 1980). Several authors have hypothesized or demonstrated that luminal fatty acids that are not recovered in the lymph are absorbed via the portal vein (Hyun et al. 1967, Mansbach et al. 1991, Vallot et al. 1985). Indeed, the low levels of lymph [3H] OA and [14C] AA recovered in the lymph of rats prefed HMCT, in comparison with rats prefed the other high-fat diets, suggested that exogenous long-chain fatty acids must have been transported by the portal vein. These results could be linked to earlier findings showing that when phosphatidylcholine was included in a high dose triolein infusion, the quantity of absorbed oleate transported in the portal vein declined from 39% to very low values (Mansbach and Dowell 1993), and that with bile diversion, both the microsomal lipid reesterifying enzyme activities and the phospholipid content of mucosal microsomes were reduced (Rodgers et al. 1973). We could therefore speculate that in rats prefed HMCT, a low biliary phospholipid output could increase the portal vein transport of exogenous long-chain fatty acids.
In the 3 h after infusion of the lipid emulsion, the composition of lymph fatty acids was influenced by the following: 1) the intestinal exogenous fatty acid lymph absorption efficiency, 2) the fatty acid composition of biliary phospholipids, and 3) the ability of the intestine to absorb bile salts and subsequently to stimulate the biliary production of phospholipids during the absorption of the lipid emulsion. These variables depend on the nature of the fat in the prefed diet and on the fatty acids examined. Studies concerning the influence of the alteration of endogenous lipids by these high-fat diets on activity and expression of some enzymes and binding proteins involved in enterocyte lipid reesterification processes are presently under investigation.
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ACKNOWLEDGMENTS |
The authors extend their thanks particularly to H. Carlier for many helpful discussions, M. C. Monnot for her skillful technical assistance, L. Sutherland from Keele University (England) for her translation assistance, Astra Calvé (Paris la Défense, France) and Zapata Protein Society (Reedville, VA) for the gift of oils.
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Abstract
Introduction
Abstract
-3) eicosapentaenoic acid.
J. Nutr.
1985;
115:219-225
