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ke Nilsson*2
*
Gastroenterology Division, Department of Medicine, Lund University, Lund, Sweden; and the
Clinical Nutrition Research Unit, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden
2To whom correspondence should be addressed. E-mail: ake.nilsson{at}med.lu.se.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • arachidonic acid • clearance • free fatty acids • retention rate • tissue uptake
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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–3
), uptake of 2-arachidonyl-lysophosphatidylcholine (2-AA-LPC) (4
), and uptake plasma unesterified arachidonic acid (FFA-AA) (5
) are assumed to be three major sources of AA for extrahepatic tissues. AA may also be transported to tissues by lipoproteins. Melin et al. (6
) showed, however, that in rats the equilibration between plasma lipoprotein AA and tissue AA seemed to be slow in several extrahepatic tissues. AA is also released at a slower rate from VLDL and chyle chylomicrons by lipoprotein lipase than other fatty acids (7
). In a review of the sources of eicosanoid precursor fatty acid pools in tissues, we calculated the AA traffic in humans as free fatty acids (FFA-AA), LPC-AA and LDL from available data on concentration and turnover rates, and found that the masses of AA cleared from blood were 3.8–7.0 mmol/d as FFA, 0.9–4.7 mmol/d as LPC-AA 0.1–0.2 mmol/d as LDL, respectively (5
). Although uptake of LDL-AA in cell cultures (8
,9
) may stimulate eicosanoid formation in vitro, the transport by LDL in vivo may, thus, be quantitatively less important. In previous studies we found that there is considerable formation of AA in the gastrointestinal tract and blood forming tissues by local interconversion of linoleic acid taken up as FFA from blood both in rats and guinea pigs (1
–3
). The concentration and composition of plasma FFA are influenced by dietary fatty acid absorption and release of individual fatty acids from adipose tissue during fasting (10
,11
). The pool size of FFA-AA in plasma is usually low (12
,13
), and different in obligate carnivores, omnivores and herbivores (3
,14
). The fates of individual FFA also differ, in that they are partitioned differently between oxidation, triglyceride (TG) synthesis and synthesis or reacylation of membrane phospholipids. Plasma FFA-AA can be taken up by several tissues and is preferentially acylated into phospholipids (6
). Murphy et al. (15
) found that 14C-AA were mainly esterified into heart phospholipids, primarily phosphatidylcholine (PC). In contrast, 14C-16:0 was esterified mainly into heart neutral lipids, primarily triglycerides (TG). However, the quantitative role of the plasma FFA-AA pool in the supply of AA to tissues has not been estimated. In this study we measured the rate of retention of FFA-AA from plasma in various tissues in rats, and report that despite the low concentration of FFA-AA this fraction supplies substantial amounts of AA not only to the liver but also to heart, skeletal muscle, bone marrow, lung and kidney phospholipids. |
MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1-14C-AA (specific activity 50 mCi/mmol) was purchased from Larodan Fine Chemicals AB (Malmö, Sweden). The labeled AA were bound to albumin in serum that was obtained from fed rats as described earlier (16
). The rats were fed with standard pellet diet R36 (Lactamin AB, Stockholm, Sweden) with 18.5 g/100 g protein (wt/wt) and 4 g/100 g (wt/wt) of fat (fatty acid composition is 16:0, 19.9 g/100 g; 16:1, 1.5 g/100 g; 18:0, 3.3 g/100 g; 18:1, 20.7 g/100 g; 18:2(n-6), 40.8 g/100 g; 18:3(n-3), 4.3 g/100 g; 20:4(n-6), 0.1 g/100 g; 20:5, 0.9; 22:1, 1.3 g/100 g; and 22:6, 1.9 g/100 g.
Male Sprague-Dawley Rats (175–220 g) were purchased from Alab (Stockholm, Sweden). They were kept under a controlled dark–light schedule and had free access to the standard diet until the time of the experiment (0900 h). Labeled serum (0.5 mL, 4 µCi 14C-AA) was injected into the jugular vein of anesthetized rats (intramuscular injection of ketamine: xylazine 2:1, 1 mL/kg). After 5 min, the rats were killed by aortic puncture. The liver, stomach, upper half of small intestine, lower half of small intestine, colon, bone marrow from two femurs, tibias and humerus, spleen, heart, lungs, kidneys, brain, testis, skeletal muscle from legs, brown adipose tissue (obtained from the backside of neck) and white adipose tissue (obtained from the subcutaneous adipose of groin) were removed and the lipids were extracted with chloroform: methanol (1:2 v/v) containing 0.05 g/L butylated hydroxy-toluene (BHT) as an antioxidant.
For determining the clearance of 14C-AA in plasma, 5 anaesthetized rats were intravenously injected with 0.5 mL of labeled serum containing 1.8 x 106 dpm 14C-AA into the jugular vein. Blood samples (0.2–0.3 mL) were obtained from an 8-cm long (0.5-mm inner diameter) catheter placed in the carotid artery at 5, 10, 15, 30, 60, 90, 120 and 180 s (the first drop of blood at all time points was avoided), with the replacement of the same amount of physiological saline. Ten microliters of plasma were counted in a Packard TriCarb 2100 liquid scintillation system (Packard Instrument Company, Meriden, CT) using the automatic external standard for quench correction, and another 50–100 µL plasma of each sample was extracted with chloroform: methanol (1:1 v/v) containing 0.05 g/L BHT. This study was approved by the District Animal Ethics Committee at Lund/Malmö.
Determination of radioactivity in different lipid classes.
After lipid extraction and two-phase distribution, aliquots of the lower phase were evaporated with nitrogen and redissolved in a small volume of chloroform for TLC. Nonpolar lipids were separated by TLC on silica gel G plates, which were developed in petroleum ether:diethyl ether:acetic acid (80:20:1, v/v). Phospholipids were separated on Merck silica gel 60 plates, which were developed in chloroform:methanol:acetic acid:water 100:80:12:1.2 (v/v). Spots were identified by staining with iodine vapor and scraped into counting vials. One milliliter methanol:water 1:1 (v/v) and 10 mL Instagel:toluene 1:1 (v/v) were added and the radioactivity of the samples was determined as described above.
Separation of plasma unesterified AA by gas chromatography.
The concentration of FFA in serum from rats was measured using an NEFA-C kit (WAKO Chemicals GmbH, Neuss, Germany), which is based on an in vitro enzymatic method for the quantitative determination of nonesterified fatty acids.
The composition of the plasma unesterified fatty acids was determined by gas liquid chromatography (GC). The extraction, separation by thin layer chromatography, and methylation of the FFA were performed as described in detail by Boberg et al. (17
). The fatty acids methyl eaters were separated by GC using a Hewlett-Packard GC system (Avondale, PA) consisting of an HP 5890 Series II GC apparatus, HP 7673 automatic sampler, HP 3365A Series Chemstation integrator software and a 50-m x 0.25-mm CP-Sil 88 Chrompack capillary column with helium as a carrying gas. Standards from Nu-Check-Prep (Elysian, Elysian, MN) were used for identification of the individual fatty acids and as a control of the GC system. The proportions of the fatty acids are given as the relative percentage of the fatty acids analyzed.
Calculations.
We used the 0-s value as the 100% as injected value. The rate of clearance was estimated by polynomial regression analysis of the amounts of total 14C radioactivity and 14C-FFA radioactivity remaining in plasma at different times. The initial half-life was calculated using the logarithm values from the percent total 14C or 14C-FFA radioactivity of the injected dose remaining in plasma plotted against time.
Based on the assumptions that the degree of 14C-AA retained in tissues is the same as that of unlabeled FFA-AA continuously taken up from the plasma FFA fraction (2
), and that deacylation followed by oxidation or tissue redistribution after the initial acylation into tissue lipids is negligible over the period studied. The rate of the retention of plasma FFA-AA in different tissues expressed as mass per time limit can then be calculated from the mass of AA that disappeared from blood and the percentage of this amount that is retained in the tissues over the period studied.
Statistical analysis.
Values are reported as the means ± SEM. Data were analyzed using row means/totals and polynomal linear regression in program of GraphPad Prism purchased from GraphPad Software (San Diego, CA).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The radioactivity left in plasma was 41.6 ± 1.5% of injected dose at 5 s after injection. At 60 s after injection, only 4.6% of the injected dose was left in plasma. At 5–30 s after injection, > 92% of the plasma 14C was in FFA, at 60–120 s, 83–89% and at 180–300 s, 66–76% (Table 1
). The remaining part of 14C was in phospholipids and diacylglycerol; very little was in water-soluble metabolites. Radioactivity in the plasma cholesterol ester and triglyceride fraction was found at 5 min after injection (Table 1)
. The initial half-life of the percentage of total 14C (Fig. 1a
) or 14C-FFA (Fig. 1
b) radioactivity of the injected dose remaining in plasma was 4.0 and 3.8 s, respectively.
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). On the assumption that the plasma volume of rats is 4% of the body weight (18
), we calculated the plasma pool of FFA-AA to be 75.7 ± 2.2 nmol. From the half-life of 3.8 s we calculated that 604 nmol/min FFA-AA is cleared from the plasma in rats.
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The rats were killed 5 min after intravenous injection of 14C-AA. The total 14C radioactivity left in serum was 0.9 ± 0.1% of injected dose at this time, of which 51.5% was in the FFA fraction. The retained 14C in different tissues at this time point is shown in Figure 2
. The 14C radioactivity per gram of tissue in the heart and lung was higher than that in other tissues but much lower than that in the liver. The total uptake of 14C-AA in whole liver was 37.4 ± 2.5% of injected dose. The total uptake in bone marrow was 6.3 ± 0.5%, in the gastrointestinal tract including stomach, upper part-, lower part-small intestine and colon was 4.7 ± 0.1% of injected dose; in lung, 3.1 ± 0.5%; kidneys, 2.7 ± 0.2%; heart, 1.8 ± 0.1%; and in spleen, 0.8 ± 0.1%.
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. The total amount of AA taken up by the liver was lower than that in the skeletal muscle.
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In most tissues, 1.4–5.4% 14C was in water-soluble metabolites, 8–13% in colon, kidney and small intestine, 16% in brain and 23% in testis. Bone marrow had the lowest proportion of 14C in water-soluble metabolites, which reflects oxidation of 14C-AA in tissues. The distribution of 14C between individual nonpolar lipids and total phospholipids (PL) is given in Tables 4
and 5
. Most 14C was incorporated into PL. The proportion of radioactivity in phospholipids was rather low in heart, and was lowest in white adipose tissue. The proportion of radioactivity in TG was higher in the heart, testis and white adipose tissue than in other tissues. A higher proportion of radioactivity in FFA found in white adipose and brain tissues (Table 4
). Among the individual phospholipids in tissues, 54–86% radioactivity was in phosphatidylcholine (PC), and the remaining part of 14C radioactivity was mainly in phosphatidylethanolamine (PE) and phosphatidylinositol (PI). However, about 25% radioactivity was found in PI and 13% in PE in brain (Table 5
). Substantial retention of radioactivity in cardiolipin occurred in heart and lung.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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–3
,16
) and in individual tissues such as the heart (3
,15
). We conclude that in fed rats the FFA-AA pathway is quantitatively more important in the supply of AA to peripheral tissues than is local interconversion of FFA-linoleic acid (1
–3
) and uptake as 2-AA-LPC (4
).
In agreement with previous studies (14
), the concentration of FFA-AA was low, 9.3 µmol/L. This may be compared with recent studies showing that the concentration of plasma unesterified AA in humans was 1,2–3,7 µmol/L (5
,12
,14
,19
). In this study, the rats were in the fed state. Other studies have shown that the FFA-AA increases less during food deprivation and physical exercise than does the plasma concentration of other FFA, probably due to the low concentration of AA in adipose tissue triglycerides (11
). AA is under-represented also among the FFA released during the action of lipoprotein lipase on TG rich lipoproteins, because it is preferentially partitioned to lipoprotein phospholipids (20
), and because the AA TG esters exhibit a partial resistance to lipoprotein lipase. AA-containing phospholipids are metabolized by hepatic lipase and LCAT, i.e., by pathways that form AA-containing LPC and cholesteryl ester but that do not release AA as FFA (5
). Collaborating factors, thus, tend to keep the FFA-AA level low.
The fractional clearance rate of plasma unesterified 14C-AA was faster than of unesterified 14C-linoleic acid observed in previous studies of rats (1
) and guinea pigs (2
,3
). The findings agree with studies in humans by Hagenfeldt et al. (21
) who found that the fractional turnover of plasma unesterified AA was 50% higher than that of oleic acid. However, the turnover of FFA-AA was not significantly increased during physical exercise, in contrast to the turnover of oleic acid. It was calculated that 1–2 g of AA is cleared every day from plasma FFA in humans, which greatly exceeds the daily dietary supply of AA (5
). Despite the low concentration of AA in the FFA fraction, this transport form may, thus, be of major importance in the supply of AA to tissue phospholipids.
Large proportions of AA taken up from blood as FFA were retained in liver, heart, lung, kidney, bone marrow, spleen, gastrointestinal tract, brown adipose tissue and skeletal muscle. Although the rate of retention per gram tissue was 
90% lower in skeletal muscle than in the liver, the retention in skeletal muscle was approximately as large due to the large mass of muscle tissue (Table 3)
. A calculation based on available data on tissue concentrations phospholipids and concentrations of AA (22
–25
) indicate that the rate of AA retention in the liver amounted to approximately one pool size (182 µmol/200 g rat) of AA per 13 h and in muscle the retention is approximately one pool size (280 µmol/200 g rat) per 19 h. In brain, the retention was low, but still 10-fold higher than in testes. This supports earlier data indicating that there is an uptake of unesterified AA by the tissues of the central nervous system.
In our previous study we found that liver-derived 2-LPC (4
) and local interconversion of linoleic acid taken up as plasma unesterified linoleic acid (1
–3
) are important sources of AA for extrahepatic tissues. The local interconversion pathway seems more important in animals with a low level of AA in plasma, e.g., guinea pigs (2
,3
,23
). However, plasma 2-LPC and unesterified AA pathways are important for animals with high levels of plasma and tissue AA (4
,23
). Table 6
compares the role of plasma unesterified AA with plasma LPC-AA and local interconversion of plasma unesterified linoleic acid in the supply of AA to tissues in rats. The plasma unesterified AA pathway transports more AA into heart, bone marrow, lung and spleen than the other two pathways (Table 6)
. In rat myocardium, the interconversion of linoleic acid is low (1
,26
), and plasma unesterified AA and LPC supply much more AA. The small intestine obtains about equal amounts of AA from plasma FFA and from 2-LPC. However, the plasma 2-LPC pathway seems to be a more important source of AA for rat brain (Table 6)
, which is in agreement with the finding that doubly labeled 2-LPC can be taken up by brain tissues without prior hydrolysis and reacylated at 1-acyl position to form membrane PC (27
), at a 6- to 10-fold higher rate than the corresponding unesterified fatty acid (27
,28
).
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and 5)
. This selective initial acylation into PC is likely to be catalyzed by the LPC-acyl- CoA-acyltransferase. This enzyme exhibits a distinct preference for AA-CoA in vitro, particularly at low acyl-CoA concentrations (29
) and also distinctly selects AA-CoA from an acyl-CoA mix (30
). A consistent finding has been that after uptake of AA into tissues, a high initial acylation into PC is followed by remodeling reactions increasing the retention, particularly in phosphatidylethanolamine (31
). In this study, we examined the tissues five minutes after injection of unesterified 14C-AA. In earlier studies we did not notice any change in tissue radioactivity or its distribution between lipid classes between 5 and 10 min (1
,2
). We, therefore, postulate that the tissue retention and distribution pattern reflects the initial acylation reactions and are influenced only to a small extent by deacylation-reacyaltion reactions during which oxidation of acyl-CoA may occur.
In conclusion, this study indicates that the plasma FFA-AA are a major source of AA in peripheral tissues of rats. There are mechanisms that keep the levels low but the turnover rate is high. A quantitatively large transport of AA can occur, still taking advantage of the high AA preference of the LPC acyl-CoA acyltransferase at low acyl-CoA concentrations and avoiding inappropriate eicosanoid formation and incorporation into TG that may occur at higher concentrations of FFA-AA. The relative importance of the three major pathways for AA supply to tissues, i.e., the FFA-AA pathway, the 2-AA-LPC pathway and the local interconversion of LA taken up as FFA can be expected to vary considerably with the nutritional state and the herbivore–carnivore status of the species examined (5
).
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FOOTNOTES |
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3 Abbreviations used: AA, arachidonic acid; CE, cholesteryl ester; FFA, free fatty acids; FFA-AA, unesterified arachidonic acid; LCAT, lecithin:cholesterol acyltransferase; LPC, lyso-phosphatidylcholine; PC, phosphatidylcholine; PE, phosphatidyl-ethanolamine; PL, phospholipids; TG, triglyceride.
Manuscript received 10 January 2002. Initial review completed 25 February 2002. Revision accepted 12 March 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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