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Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Triton WR1339, an Inhibitor of Lipoprotein Lipase, Decreases Vitamin E Concentration in Some Tissues of Rats by Inhibiting Its Transport to Liver¹

² Department of Nutritional Sciences, Nagoya University of Arts and Sciences, Nissin 470-0196, Japan; ³ Department of Food and Nutrition, Sugiyama Jogakuen University, Nagoya 464-8662, Japan

^* To whom correspondence should be addressed. E-mail: saiko{at}nuas.ac.jp.

	ABSTRACT

TOP ABSTRACT Introduction Materials and Methods Results Discussion LITERATURE CITED

 
The aim of this experiment was to clarify the contribution of the -tocopherol transfer activity of lipoprotein lipase (LPL) to vitamin E transport to tissues in vivo. We studied the effect of Triton WR1339, which prevents the catabolism of triacylglycerol-rich lipoproteins by LPL on vitamin E distribution in rats. Vitamin E-deficient rats fed a vitamin E-free diet for 4 wk were injected with Triton WR1339 and administered by oral gavage an emulsion containing 10 mg of -tocopherol, 10 mg of -tocopherol, or 29.5 mg of a tocotrienol mixture with 200 mg of sodium taurocholate, 200 mg of triolein, and 50 mg of albumin. -Tocopherol was detected in the serum and other tissues of the vitamin E-deficient rats, but -tocopherol, - and -tocotrienol were not detected. Triton WR1339 injection elevated (P < 0.05) the serum -tocopherol concentration and inhibited (P < 0.05) the elevation of -tocopherol concentration in the liver, adrenal gland, and spleen due to the oral administration of -tocopherol. Neither -tocopherol administration nor Triton WR1339 injection affected (P 0.05) the -tocopherol concentration in the perirenal adipose tissue, epididymal fat, and soleus muscle despite a high expression of LPL in the adipose tissue and muscle. These data show that -tocopherol transfer activity of LPL in adipose tissue and muscle is not important for -tocopherol transport to the tissue after -tocopherol intake or that the amount transferred is small relative to the tissue concentration. Furthermore, Triton WR1339 injection tended to elevate the serum -tocopherol (P = 0.071) and -tocotrienol (P = 0.053) concentrations and lowered them (P < 0.05) in the liver and adrenal gland of rats administered -tocopherol or -tocotrienol. These data suggest that lipolysis of triacylglycerol-rich chylomicron by LPL is necessary for postprandial vitamin E transport to the liver and subsequent transport to the other tissues.

	Introduction

TOP ABSTRACT Introduction Materials and Methods Results Discussion LITERATURE CITED

Dietary vitamin E isoforms are absorbed in the intestine and carried to the liver as a result of the uptake of chylomicron remnants (4). There is no discrimination between -tocopherol and other isoforms during absorption and chylomicron secretion by the intestine (5,6). -Tocopherol transfer protein (-TTP),⁴ tocopherol-associated protein, and tocopherol-binding protein have been reported to be the tocopherol-regulatory proteins that determine tissue tocopherol levels (7,8). It is thought that -TTP plays an important role in the discrimination of vitamin E isoforms. -TTP catalyzes -tocopherol secretion by a non-Golgi-mediated pathway in liver cells, and -tocopherol is incorporated into VLDL and subsequently transported to the various tissues by lipoproteins (9). The other isoforms of vitamin E such as -tocopherol and tocotrienol are metabolized and excreted because their affinity for -TTP is much lower than that of -tocopherol. The importance of -TTP for the vitamin E distribution is supported by the extremely low level of -tocopherol in plasma of the patients who have ataxia with vitamin E deficiency due to mutations in the -TTP gene (10) and in plasma and various tissues of -TTP-knockout mice (11,12).

The discrimination of vitamin E isoforms by -TTP, however, does not completely explain the tissue-specific accumulation of tocotrienol. - and -Tocotrienol preferentially accumulate in the adipose tissue of rats fed a diet containing - and -tocotrienol for 8 wk, whereas -tocopherol accumulates in the various tissues and plasma (13,14). Little is known about the precise mechanism of tocotrienol transport to the adipose tissue. Some reports suggest that lipoprotein lipase (LPL) is responsible for the transfer of -tocopherol in vitro and in vivo. Exogenous bovine LPL transferred -tocopherol to human fibroblasts (15) or rat skeletal muscle myoblasts (16). Muscle-specific overexpression of LPL elevated the -tocopherol concentration in the muscle of transgenic mice (17). Furthermore, the -tocopherol concentration in the brain of LPL-knockout mice was lower than that of the control mice (18). These results suggest that LPL contributes the transfer of -tocopherol associated with triacylglycerol-rich lipoproteins, such as chylomicrons and VLDL, to some tissues expressing LPL.

Adipose tissue is a major tissue expressing LPL and takes up fatty acids derived from dietary triacylglycerol by high LPL lipolytic activity. To clarify the contribution of LPL to tocopherol and tocotrienol distribution in vivo, we studied the effect of Triton WR1339, a nonionic detergent that prevents the catabolism of triacylglycerol-rich lipoprotein by LPL (19–21) on the tocopherol or tocotrienol concentration in the tissues of rats after oral administration of tocopherol or tocotrienol.

	Materials and Methods

TOP ABSTRACT Introduction Materials and Methods Results Discussion LITERATURE CITED

 
    Materials. Vitamin E used for oral administration and used as standards were generously donated by Eisai. The tocotrienol mixture composition was 339 mg/g -tocotrienol, 40 mg/g ß-tocotrienol, 471 mg/g -tocotrienol, and 110 mg/g -tocotrienol. Triton WR1339 was purchased from Sigma.

    Animals and diets. Male Wistar rats (6 wk of age) were purchased from Japan SLC (Shizuoka) and maintained at 23°C with a 12-h light cycle (lights on from 0800 to 2000). Before the start of the experiment, rats were fed a vitamin E-free diet (Table 1), for 4 wk to deplete tissue vitamin E stores. This study was approved by the Laboratory Animal Care Committee of Nagoya University of Arts and Sciences, and all procedures were performed in accordance with the Animal Experimentation Guidelines of Nagoya University of Arts and Sciences.

    Lipid concentrations. Lipids were extracted from liver using chloroform:methanol (2:1). Triacylglycerol and cholesterol concentrations in the serum and liver were measured with the Triglyceride E-Test Wako (Wako Pure Chemical Industries) and the Cholesterol E-Test Wako (Wako Pure Chemical Industries), respectively.

    Vitamin E concentration. Tissues were homogenized in distilled water. The tissue homogenate (0.5 mL) was put in a test tube, and 0.5 mL of ethanol containing 60 g/L pyrogallol and 0.45 µg of 2,2,5,7,8-pentamethyl-6-chroman as an internal standard were added. Then, 0.1 mL of 600 g/L potassium hydroxide was added and saponified at 70°C for 30 min. After the addition of 2.25 mL of 20 g/L sodium chloride, tocopherols and tocotrienols were extracted with 0.5 mL of hexane containing 10% (v:v) ethyl acetate. Serum (75 µL) was put in a test tube, and 90 ng of 2,2,5,7,8-pentamethyl-6-chroman as an internal standard was added. After the addition of 0.5 mL of water and 1.0 mL of ethanol, vitamin E was extracted with 5 mL of hexane.

Vitamin E concentration was determined by HPLC (23). The instrumentation used for HPLC was a Shimadzu LC-10AD (Shimadzu) with a Shimadzu RF-10AXL fluorescence detector (excitation 298 nm, emission 325 nm). The analytical column used was a Develosil 60–5 (4.6 x 250 mm, Nomura Chemical). The mobile phase was hexane containing 1% (v:v) dioxane and 0.2% (v:v) isopropyl alcohol with a flow rate of 1 mL/min.

    Statistical analysis. Data are presented as means ± SEM, n = 4–8. They were analyzed by 2-way ANOVA with Tukey's post-hoc test (24) (Graph Pad Prism for Windows, version 4.0, GraphPad Software). When variances among groups were unequal, the data were logarithmically transformed before analysis by 2-way ANOVA. Differences were regarded as significant at P < 0.05.

	Results

TOP ABSTRACT Introduction Materials and Methods Results Discussion LITERATURE CITED

 
The serum triacylglycerol concentration in rats intravenously injected with Triton WR1339 at 2, 4, 6, and 8 h after oral administration of triacylglycerol was higher (P < 0.05) than that at 0 h, although the triacylglycerol concentrations in rats intraperitonealy injected with Triton WR1339 at 0, 2 and 4 h did not differ (P 0.05) (Fig. 1). The triacylglycerol concentration in rats injected intravenously was higher (P < 0.05) than that in rats injected intraperitonealy at 4, 6, and 8 h.

View larger version (10K): [in this window] [in a new window]   Figure 1  Effect of intravenous (iv) or intraperitoneal (ip) injection of Triton WR1339 on serum triacylglycerol concentration in rats. At 10 min after the Triton WR1339 injection, the rats were administered an oral gavage of 1 mL of emulsion containing 200 mg of triolein, 200 mg of sodium taurocholate, and 50 mg of albumin. The triacylglycerol concentration at 0 h was 0.50 ± 0.15 mmol triolein/L. Values are means ± SEM, n = 6 (iv) or 3 (ip). There were effects of route (P < 0.001), time (P < 0.001), and their interaction (P < 0.001). Means not sharing a letter differ, P < 0.05.

View this table: [in this window] [in a new window]   TABLE 3 -Tocopherol concentration in serum and tissues of rats administered a vitamin E-free emulsion, -tocopherol, Triton, or -tocopherol + Triton1

View this table: [in this window] [in a new window]   TABLE 4 -Tocopherol concentration in serum and tissues of rats administered a vitamin E-free emulsion, vitamin E, Triton, or vitamin E + Triton1

	Discussion

TOP ABSTRACT Introduction Materials and Methods Results Discussion LITERATURE CITED

 
To clarify the contribution of LPL to tocopherol or tocotrienol distribution in vivo, the effect of Triton WR1339 on the tocopherol or tocotrienol concentration in the tissue of rats after oral administration of tocopherol or tocotrienol was studied. Triton WR1339 is a nonionic detergent that prevents catabolism of triacylglycerol-rich lipoproteins by LPL (19–21) and is commonly used for the in vivo determination of triacylglycerol production, and VLDL secretion or clearance rate. Intravenous injection of Triton WR1339 linearly elevated the serum triacylglycerol concentration until 6 h after oral administration of triacylglycerol (Fig. 1). The serum triacylglycerol and cholesterol concentrations were elevated by Triton WR1339 injection at 6 h after the oral administration of vitamin E (Table 2). Thus, Triton WR1339 prevents the lipolysis of triacylglycerol-rich lipoproteins by LPL after oral administration of triacylglycerol.

Oral administration of 10 mg of -tocopherol elevated the serum -tocopherol concentration of the vitamin E-deficient rats (Table 3). Triton WR1339 injection elevated the serum -tocopherol concentration of rats administered -tocopherol. A large amount of triacylglycerols also accumulated in the serum by Triton WR1339 (Table 2). These data suggest that LPL contributes to the transport of dietary -tocopherol to some tissues. The oral administration of -tocopherol elevated the -tocopherol concentration in the liver, adrenal gland, spleen, lung, heart, and thymus (Table 3). However, Triton WR1339 completely inhibited the elevation of the -tocopherol concentration in the liver, adrenal gland, and spleen by -tocopherol administration. These data indicate that Triton WR1339 inhibits -tocopherol transport to the liver and subsequent transport to the other tissues after oral administration of -tocopherol. This result suggests that lipolysis of triacylglycerol-rich chylomicrons by LPL is necessary for postprandial -tocopherol transport to the liver and subsequent transport to the other tissues. Chylomicrons with dietary triacylglycerol secreted from the intestine changes chylomicron remnant as a result of the lipolysis of chylomicron triacylglycerols by LPL at the tissues that highly express LPL, and then chylomicron remnant is transported to the liver through remnant receptor. The data suggest that remnant receptor cannot uptake triacylglycerol-rich chylomicrons into the liver.

The major tissues that highly express LPL are adipose, heart, skeletal muscle, lung, and aorta. In addition, Goti et al. (18) suggested that LPL contributes to the uptake of -tocopherol associated with LDL to the brain. In this study, -tocopherol administration elevated the -tocopherol concentration in the lung and heart but did not significantly elevate the -tocopherol concentration in the perirenal adipose tissue, epididymal fat, muscle, aorta, and brain 6 h after oral administration of -tocopherol (Table 3). The elevation of the -tocopherol concentration in the adipose tissue, muscle, and brain by oral administration of -tocopherol is very slow or the amount transferred is small relative to the tissue concentration, because the -tocopherol concentrations in the adipose tissue, muscle, and brain until 24 h after oral administration of -tocopherol were not different from those before the -tocopherol administration (data not shown). Therefore, oral -tocopherol is preferentially transported to the liver, adrenal gland, spleen, and lung for 6 h, and the -tocopherol concentrations in the adipose tissue, muscle, aorta, and brain are difficult to influence by oral -tocopherol administration. LPL contribution to dietary -tocopherol transport to the adipose tissue, muscle, aorta, and brain may be limited in this study, although LPL has -tocopherol transfer activity in some experimental conditions (15–18).

The effect of Triton WR1339 injection on the distribution of vitamin E isoforms as well as -tocopherol was examined. Triton WR1339 injection tended to elevate the serum -tocopherol (P = 0.071) or -tocotrienol (P = 0.053) concentration of rats administered 10 mg of -tocopherol or a tocotrienol mixture containing 10 mg of -tocotrienol (Table 4). Triton WR1339 injection lowered the -tocopherol concentration in the liver, adrenal gland, and the -tocotrienol concentration in the liver, adrenal gland, lung, and muscle. These findings suggest that transport of not only -tocopherol, but also -tocopherol or -tocotrienol, to the liver and subsequent transport to the other tissues requires lipolysis of chylomicron triacylglycerol by LPL. The -tocotrienol concentration in the serum, adrenal gland, and lung of rats administered tocotrienol mixture without Triton WR1339 was lower than the -tocotrienol concentration in those tissues, although the dose amount of -tocotrienol (14 mg) was more than that of -tocotrienol (10 mg). Triton WR1339 injection did not significantly affect the -tocotrienol concentration. Ikeda et al. (6) reported that the absorption rate from the intestine to the lymph of -tocotrienol and -tocopherol in rats did not differ. -Tocotrienol may be metabolized and excreted faster than the other isoforms.

We have studied the tissue-specific distribution of tocotrienol in rats (13,14,25). The dietary -tocotrienol accumulated in some tissues, including kidney, heart, lung, muscle, adipose tissue, and skin of rats fed a diet containing -tocotrienol without other vitamin E isoforms for 8 wk. The dietary -tocotrienol preferentially accumulated in the adipose tissue and skin of rats fed a diet containing -tocotrienol with -tocopherol for 8 wk, and the -tocotrienol concentration in the other tissues was very low. The dietary -tocotrienol accumulated in the adipose tissue and skin of rats fed a diet containing -tocotrienol with or without -tocopherol for 8 wk. Thus, the dietary intake of - and -tocotrienol for a long period, like 8 wk, elevates the - and -tocotrienol concentrations in the adipose tissue and skin tissue specifically. However, the - and -tocotrienol concentrations in the adipose tissue and skin at 6 h after the oral administration of tocotrienol mixture were not higher than those in some tissues, including liver, adrenal gland, spleen, and lung (Table 4). These data indicate that the dietary - and -tocotrienol do not preferentially transport to the adipose tissue and skin just after tocotrienol intake but gradually accumulates in those tissues by its daily intake over a long period. The -tocopherol concentration in the adipose tissue may be too high or the amount of adipose tissue too large to see the changes in the tocotrienol concentration.

Minehira-Castelli et al. (26) recently showed that HDL, not VLDL, played an important role in the tocopherol transport to the peripheral tissue in microsomal triacylglycerol transfer protein-deficient (VLDL-deficient) mice. Triton WR1339 injection did not affect the HDL triacylglycerol concentration but rapidly removed apolipoprotein A-I from HDL particle (27,28). Scavenger receptor class B type I deficiency lowered the -tocopherol concentration in some tissues of mice with the elevation of the -tocopherol concentration in the plasma (29). These data show the possibility that Triton WR1339 inhibits not only lipolysis of chylomicron and VLDL triacylglycerol by LPL but also in part -tocopherol transfer from HDL to some tissues by scavenger receptor class B type I that is associated with apolipoprotein A-I. HDL is a major lipoprotein that contains large amount of -tocopherol in rats and mice. Further study about the effect of HDL metabolism on -tocopherol transport to the tissues may be needed.

In conclusion, the present study suggests that lipolysis of triacylglycerol-rich chylomicrons by LPL is necessary for postprandial transport of -, -tocopherol, and -tocotrienol to the liver and subsequent transport to the other tissues such as adrenal gland, spleen, and lung. LPL contribution to the vitamin E transport to the adipose tissue and muscle may be limited due to the small amount transferred after the administration.

	FOOTNOTES

 
¹ Supported in part by Grant-in-Aid for Scientific Research 15680018 from Japan Society for the Promotion of Science, Japan.

⁴ Abbreviations used: LPL, lipoprotein lipase; T, rats administered -tocopherol; T, rats administered -tocopherol; T3, rats administered tocotrienol mixture; Tr, rats injected with Triton WR1339 and administered vitamin E-free emulsion; -TTP, -tocopherol transfer protein; T + Tr, rats injected with Triton WR1339 and administered -tocopherol; T + Tr, rats injected with Triton WR1339 and administered -tocopherol; T3 + Tr, rats injected with Triton WR1339 and administered a tocotrienol mixture.

Manuscript received 15 September 2006. Initial review completed 19 October 2006. Revision accepted 28 November 2006.

	LITERATURE CITED

TOP ABSTRACT Introduction Materials and Methods Results Discussion LITERATURE CITED

 

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This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Abe, C. Articles by Ichikawa, T. Search for Related Content PubMed PubMed Citation Articles by Abe, C. Articles by Ichikawa, T.