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Department of Biological Resources, Faculty of Agriculture, Ehime University, Matsuyama 790-8566, Japan and * Department of Hygiene, Kinki University, School of Medicine, Osaka 589-8511, Japan
2To whom correspondence should be addressed. E-mail: ebihara{at}agr.ehime-u.ac.jp.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-hydroxylase activity (P < 0.01) and fecal bile acid excretion (P < 0.01). Taurine increased the HMG-CoA reductase mRNA level (P < 0.02) in the liver of rats fed coconut oil, but not in those fed corn oil. Taurine increased liver total lipid (P < 0.05) and triglyceride (P < 0.05) concentrations in rats fed corn oil, but not in those fed coconut oil. These results indicate that the effect of taurine on ovarian hormone deficiency–induced changes in cholesterol metabolism is influenced by the type of dietary fatty acids.
KEY WORDS: • ovariectomy • taurine • fatty acid • plasma cholesterol • rats
Menopause, whether natural or surgically induced, is associated with elevated levels of circulating total cholesterol and LDL cholesterol (LDL-C), placing postmenopausal women at greater risk for coronary heart disease (CHD) (1–4). These changes are a consequence of the reduction in the level of circulating estrogen. The mechanism through which a reduced level of circulating estrogen elevates the plasma cholesterol level is poorly understood. Reductions in the activity of hepatic LDL receptors (LDLR) (5–7) and/or cholesterol 7-hydroxylase (CYP7) activity (8,9) are presumably involved.
Numerous studies suggest that taurine, 2-amino ethane sulfonic acid, has beneficial effects on cholesterol metabolism by improving the effects that hypercholesterolemia exerts (10–13). Taurine up-regulated LDLR activity in a human hepatoma cell line (14) and in hamsters (15). Therefore, up-regulation of hepatic LDLR activity may be involved in the hypocholesterolemic effect of taurine. Estrogen replacement therapy (ERT) in postmenopausal women reduces the risk of CHD in part by modulating serum cholesterol. However, ERT and cholesterol-lowering pharmacologic agents may be accompanied by side effects. On the other hand, taurine is thought to be quite safe and there is little concern about the side effects of excessive intake of taurine (16).
It has also been shown that different types of dietary fatty acids have different effects on the concentration of circulating LDL-C in animals (17,18) and humans (19,20). Feeding animals different types of fat in the diet modulates the expression of LDLR in the liver. Presumably, different dietary fatty acids influence the concentration of circulating LDL-C by changing the level of hepatic LDLR activity, the LDL-C production rate or both. Among the saturated fatty acids (SFA), only lauric, myristic and palmitic acids (12:0, 14:0 and 16:0, respectively) reduce the level of hepatic LDLR activity, whereas oleic and linoleic acids (18:1 and 18:2, respectively) increase it and stearic acid (18:0) has no effect (21).
Taurine and SFA such as lauric, myristic and palmitic acids compete with one another in the regulation of LDLR. If the preventive effect of taurine on ovarian hormone deficiency–induced hypercholesterolemia is mediated by up-regulation of LDLR activity, the effect of taurine may be negated by SFA such as lauric, myristic and palmitic acids and may be increased by oleic and linoleic acids.
Therefore, in this study we examined in ovariectomized (OVX) rats whether the preventive effect of taurine on ovarian hormone deficiency–induced hypercholesterolemia differs with the type of dietary fatty acid. We used coconut oil, rich in lauric, myristic and palmitic acids, and corn oil, rich in oleic and linoleic acids as dietary fat sources.
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MATERIALS AND METHODS |
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This study was approved by the Laboratory Animal Care Committee of Ehime University, and the rats were maintained in accordance with the Guidelines for the Care and Use of Laboratory Animals of Ehime University. Retired breeder female Wistar rats (6 mo old; Nippon SLC, Shizuoka, Japan) were used in this experiment. The rats were fed a commercial solid diet (MF, Oriental Yeast, Osaka, Japan) for 7 d. They were housed in individual cages with stainless steel screen bottoms in a room maintained at 23 ± 1°C with a 12-h light:dark cycle (light, 0700–1900h). After acclimation, bilateral OVX was performed under anesthesia by intraperitoneal injection of sodium pentobarbital (Nembutal, 30 mg/kg body; Abbott, North Chicago, IL). Rats were fed the commercial solid diet during the 7-d recovery period. After recovery, the OVX rats were divided into four groups of 6 rats each on the basis of body weight and were allowed free access to one of the following diets for 28 d: the Corn, Corn-T, Coconut or Coconut-T with or without taurine (T). The Corn and Corn-T diets contained corn oil, which is rich in linoleic acid, as the dietary fat source and the Coconut and Coconut-T diets contained coconut oil, rich in lauric and myristic acids. The compositions of the diets are shown in Table 1. The Corn-T and Coconut-T diets contained 50 g of taurine/kg diet with reductions in the carbohydrate source, i.e., sucrose and gelatinized cornstarch, by 25 g/kg diet each. The rats had free access to the respective diet and water for 28 d. Food intake was recorded daily for each rat in the morning before replenishing the diet. The body weight of each rat was measured every 7 d.
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Chemical analysis.
The levels of triglyceride (TG) and phospholipids in the plasma were enzymatically determined with commercial kits (Triglyceride E-Test Wako and Phospholipids C-Test Wako, Wako Pure Chemical Industries, Osaka, Japan). Plasma lipoprotein fractions [VLDL, d < 1.006 kg/L; LDL, d:1.006–1.063 kg/L; and HDL, d:1.063–1.210 kg/L] were separated by stepwise density-gradient ultracentrifugation (TL-100, Beckmann Instruments, Palo Alto, CA) as described below. The concentrations of total cholesterol in the plasma and cholesterol in each lipoprotein fraction were determined enzymatically with a commercial kit (Cholesterol E Test Wako, Wako Pure Chemical Industries).
The level of liver total lipids was determined gravimetrically after extraction by the method of Folch et al. (23). The levels of liver TG, total cholesterol and CYP7 activity were determined enzymatically as previously described (24). Steroids were extracted from feces by a mixture of chloroform:methanol (1:1, v/v) at 70°C for 60 h (25). The concentration of total bile acids in the feces was also determined enzymatically as previously described (24).
Plasma lipoproteins were isolated by ultracentrifugation according to the method of Hatch (26) with a slight modification. Briefly, for VLDL separation, 0.3 mL of 1.006 kg/L sodium chloride density solution was added to 0.6 mL of serum in a polycarbonate tube of the Beckman TL-100.2 rotor (Beckmann Instruments). Ultracentrifugation was performed in a Beckman TL-100 ultracentrifuge at 100,000 x g at 12°C for 2.5 h, and the VLDL layer was removed from the top. Then, the middle layer in the tube (0.15 mL) was removed, and the bottom layer in the tube (0.6 mL) was transferred to another tube. For LDL separation, 0.3 mL of 1.006 kg/L sodium bromide density solution was added to the tube, mixed and ultracentrifuged under the above conditions, and the LDL layer was removed from the top. Then, the middle layer in the tube (0.15 mL) was removed, and the bottom layer in the tube (0.6 mL) was transferred to another tube. For HDL separation, 0.3 mL of 1.478 kg/L sodium bromide density solution was added to the bottom 0.6 mL in the tube, mixed, and ultracentrifuged at 100,000 x g at 12°C for 4 h, and the HDL layer was removed from the top. All sodium bromide density solutions contained 0.5 mL of 0.5 mol/L Na2EDTA. The concentration of cholesterol in each lipoprotein fraction was determined enzymatically with a commercial kit (Cholesterol E Test Wako).
The concentrations of apolipoproteins (apo A-I, A-IV, B and E) were estimated by rocket immunoelectrophoresis according to the method of Laurell (27) with a slight modification. Briefly, serum (2 µL) that had been diluted to an adequate concentration with electrophoresis buffer containing Triton X-100 (0.01 kg/L buffer), was applied on the agarose gel (0.01 kg/L, SeaKem LE agarose, Marine Colloids Division, FMC, Rockland, NY) plate containing antiserum (125µL of anti-apo A-I, 150 µL of anti-apo A-IV, 150 µL of anti-apo B or 300 µL anti-apo E /9 mL agarose gel solution) and subjected to electrophoresis in 0.0148 mol/L Barbital/0.075 mol/L Tris-glycine buffer (pH 8.8) containing Triton X-100 (0.001 kg/L buffer) at 8.4 V/cm at 14–16°C for 3 h for apo A-I and E, or for 4 h for apo A-IV and B.
Hepatic mRNA.
Total RNA was isolated from the liver according to the method described by Chomczynski and Sacchi (28), and 15 µg of total RNA was subjected to Northern blot hybridization. The cDNA fragments used in the synthesis of RNA probes were as follows: the fragment corresponding to +2521 to +2874 of rat LDL receptor cDNA (Sawady Technology, Tokyo, Japan) and the fragment corresponding to +576 to +960 of rat 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase cDNA (Sawady Technology). The cDNA fragments were subcloned to pGEM-T Easy Vector (Promega, Madison, WI), and RNA probes were synthesized with the Dig RNA labeling kit (SP6/T7) (Roche Molecular Biochemicals, Tokyo, Japan) and used for hybridization. The RNA probe of human ß-actin was used as a normalization standard. The specific hybridization was detected by the Dig Luminescent Detection kit (Roche Molecular Biochemicals) and the membrane was exposed to X-ray film at room temperature for 30 min. The autoradiographs were scanned and determined densitometrically relative to mRNA levels with image analyzer (Fluors-S Max Malti Imager A1 system, Japan Biolab Laboratories, Tokyo, Japan).
Statistical analysis.
Data are expressed as means ± SEM. The statistical significance of differences among the groups was evaluated by two-way ANOVA, using a computer software package (StatView Version 4.5, Abacus Concepts, Berkeley, CA). Individual comparisons were made by Duncan’s new multiple range test using the Super ANOVA statistical software package (Abacus Concepts). Differences were considered to be significant at P < 0.05.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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activity and fecal bile acid excretion were significantly increased by taurine (Table 3, Fig. 1).
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The concentration of liver total lipids in OVX rats fed the coconut diet was significantly higher than that in those fed the corn diet, which was due primarily to the change in the liver TG concentration. Takeuchi et al. (32) showed that the concentration of liver TG is controlled by the type of dietary fat through differences in the hepatic enzyme activities related to fatty acid synthesis and lipogenesis. Dietary PUFA markedly reduced the levels of total and active pyruvate dehydrogenase complex (PDC), which plays a key role in the regulation of hepatic lipogenesis by dietary factors (33). On the contrary, dietary SFA did not inhibit the elevation in total PDC activity (33). Park et al. (34) showed that taurine reduced the hepatic TG concentration in rats. Yan et al. (35) also showed that taurine lowered the liver concentrations of total lipids and TG in rats. In the present study, however, taurine significantly increased the liver concentrations of total lipids and TG in OVX rats fed corn oil, whereas taurine tended to increase (P = 0.121) the liver concentration of total lipids and to reduce (P = 0.094) the liver TG concentration in OVX rats fed coconut oil. The reason for this discrepancy is unknown. On the other hand, when fed with both types of dietary fat, taurine reduced the concentration of phospholipids in the liver, which is in agreement with the results of Yan et al. (35) and Cantafora et al. (36).
The activity of acyl-CoA:cholesterol acyltransferase (ACAT) was increased in rats fed (n-6) PUFA but not in rats fed SFA (37,38). Bravo et al. (39) showed that feeding rats (n-6) polyunsaturated fat compared with saturated fat promotes the storage of cholesterol ester in the liver. In the present study, however, the liver concentration of esterified cholesterol did not differ between rats fed corn or coconut oil. On the other hand, taurine significantly increased the liver concentration of esterified cholesterol in OVX rats fed coconut oil, but not in those fed corn oil. In the liver, cholesterol is stored chiefly as the fatty acid ester. Taurine increased the level of HMG-CoA reductase mRNA in OVX rats fed coconut oil, but not in those fed corn oil. Therefore, the taurine-induced increase in the esterified cholesterol concentration in the liver of OVX rats fed coconut oil may reflect increased cholesterol synthesis in the liver. However, Murakami et al. (10) showed that taurine reduced the concentration of hepatic cholesterol ester and diminished the activity of hepatic ACAT in male stroke-prone spontaneously hypertensive young rats fed a hypercholesterolemic diet containing cholesterol and cholic acid. Also, in young male rats fed a cholesterol-free diet, dietary taurine reduced the concentration of hepatic cholesterol ester (38) and reduced the ACAT activity (36). Murakami et al. (10) used suet as the dietary fat source. The fat sources used by Yan et al. (35) and Cantafora et al. (36) are not known. Different results may have been obtained in these studies because different dietary fat sources may have been used.
Whole-body cholesterol homeostasis is controlled by supply and removal pathways. The liver is the main organ involved in the regulation of cholesterol homeostasis. Cholesterol can be excreted into the bile directly or after conversion to bile acids. In rats fed corn oil, olive oil or coconut oil, bile flow and biliary cholesterol secretion were not differentially influenced by the type of dietary fat (39,40). Taurine did not increase the biliary cholesterol output in rats (35) or in hamsters (41). Therefore, taurine would not increase the biliary cholesterol output, although the outputs of cholesterol into bile and feces were not measured in this study. The conversion of cholesterol to bile acids is an irreversible and terminal process of cholesterol catabolism. Bile acid synthesis occurs exclusively in the liver, and CYP7 is the first and rate-limiting enzyme of this pathway. We previously reported that taurine increased the activity of CYP7 and the fecal excretion of bile acids in OVX rats (42). This is consistent with the results of Cantafora et al. (36) and the present study. Bile acids are derived from hepatic cholesterol originating from plasma lipoprotein cholesterol and from de novo cholesterol synthesis (43). The liver takes up plasma lipoprotein through a receptor. Taurine up-regulates LDLR in Hep G2 cells, a human hepatoma cell line (14). The level of LDLR activity is correlated with the level of hepatic LDLR mRNA (44). In the present study, taurine significantly increased the LDLR mRNA level in rats fed both fat diets. In rats fed coconut oil, taurine increased the level of HMG-CoA reductase mRNA. Therefore, the finding that taurine increased fecal excretion of bile acids indicates increased de novo cholesterol synthesis and/or increased recovery of plasma lipoprotein cholesterol.
Several studies have suggested that taurine increases cholesterol elimination from the body by stimulating bile acid synthesis, thereby reducing the plasma cholesterol concentration (13,15,45). In rats fed corn oil, taurine increased fecal bile acid excretion and had a hypocholesterolemic effect. In rats fed coconut oil, however, taurine did not have a hypocholesterolemic effect even though it increased fecal bile acid excretion. This discrepancy may be due to a difference in the level of de novo cholesterol synthesis in the liver. In fact, taurine increased the HMG-CoA reductase mRNA level in rats fed coconut oil, but not in those fed corn oil. However, although the HMG-CoA reductase mRNA level was higher in rats fed the coconut oil diet than in those fed the corn oil diet, the plasma and liver cholesterol concentrations did not differ between the two groups. Therefore, this discrepancy cannot be explained solely by the difference in the level of HMG-CoA reductase mRNA.
In conclusion, taurine prevented ovarian hormone deficiency–induced hypercholesterolemia in rats fed corn oil, but did not in those fed coconut oil. This difference may exist because corn oil increased the up-regulation of LDLR activity by taurine, but coconut oil negated it. More detailed research is necessary to explain why the effectiveness of taurine in reducing the plasma cholesterol concentration in ovarian hormone deficiency–induced hypercholesterolemia depends on the type of dietary fat.
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FOOTNOTES |
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3 Abbreviations used: ACAT, acyl-CoA:cholesterol acyltransferase; CHD, coronary heart disease; CYP7, cholesterol 7-hydroxylase; ERT, estrogen replacement therapy; HDL-C, HDL cholesterol; HMG-CoA reductase, 3-hydroxy-3-methylglutaryl CoA reductase; LDL-C, LDL cholesterol; LDLR, LDL receptor; OVX rat, ovariectomized rat; PDC, pyruvate dehydrogenase complex; SFA, saturated fatty acids; TG, triglyceride; VLDL-C, VLDL cholesterol.
Manuscript received 6 February 2003. Initial review completed 18 March 2003. Revision accepted 12 May 2003.
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LITERATURE CITED |
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