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The Journal of Nutrition Vol. 128 No. 7 July 1998,
pp. 1084-1091
Unité de Nutrition Cellulaire et Métabolique, Faculté des Sciences Mirande, 21011 Dijon Cedex, France
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ABSTRACT |
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Abstract
Introduction
Methods
Results
Discussion
References
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The specific effects of soybean protein on lipid metabolism were determined with highly purified soybean protein. At 5 wk of age, growing rats were fed diets containing 20% highly purified soybean protein or casein supplemented or not with 0.1% cholesterol for 2 mo. Plasma and liver lipid composition, fecal steroid excretion and several hepatic enzyme activities were measured. There were no significant dietary protein-related differences in plasma and liver cholesterol concentrations. When diets were cholesterol free, highly purified soybean protein stimulated fecal neutral and acidic steroid excretion associated with concomitantly higher hydroxy methylglutaryl CoA (HMG-CoA) reductase activity, but lower cholesterol 7
-hydroxylase activity. Soybean protein lowered the linoleate desaturation index [20:4(n-6)/18:2(n-6)] in liver microsomal lipids and phospholipids. This may have been due to the reduced microsomal 
6(n-6) desaturase activity in rats fed soybean protein, whereas 5(n-6) desaturase activity did not differ between groups fed the two proteins. Cholesterol supplementation (0.1%) did not affect plasma cholesterol but increased liver cholesterol and triacylglycerol concentrations and reduced HMG-CoA reductase activity; this latter effect was greatest in rats fed soybean protein. Cholesterol 7-hydroxylase activity, however, was diminished only in rats fed casein. Desaturase activities, and particularly 5(n-6) activity, were lowered by cholesterol supplementation in rats fed both protein diets, including a significantly lower 20:4(n-6)/18:2(n-6) ratio in liver microsomal lipids and liver phospholipids. Thus although dietary proteins have no effect on serum cholesterol in rats, they affect enzyme activities involved in cholesterol metabolism and fatty acid desaturation.
casein
The importance of dietary protein in the regulation of cholesterol metabolism has been well established in various species including humans and rats (reviewed by Huang et al. 1993 In this study, we investigated the hypothesis that non-protein components of soybean protein may affect cholesterol metabolism. Although the hypocholesterolemic effect of soybean protein has been demonstrated in humans and a variety of animal models, the variable purity of vegetable protein used is questionable. Thus excluding non-protein components is essential before the possible mechanisms through which the protein components of the mixture could influence serum cholesterol concentration are explored. Therefore we investigated the effects of highly purified soybean protein (98%) vs. casein with or without the addition of 0.1% cholesterol to mimic physiological amounts, on plasma and liver cholesterol contents, fecal steroid excretion and liver enzymes involved in cholesterol metabolism (HMG-CoA reductase and cholesterol 7 Highly purified soybean protein preparation.
Soyamin 50T (53% protein and 2% lipid), purchased from Lucas Meyer (Saint Maur les Fossés, France) was diluted (100 g/L) in water containing sodium sulfite (10 mmol/L); the pH was adjusted to 10 with 1 mol/L NaOH. After sedimentation for 12 h at 4°C, the supernatant was obtained and brought to pH 4.5 with 5 mol/L H2SO4. Protein was removed after centrifugation (3000 × g for 20 min), then rinsed with distilled water. The pellet was dried at 37°C for 10 d. The purity of soybean protein was at least 98%. This purified protein may have still contained isoflavones because their removal requires an aqueous alcohol extraction process. However, their quantities were probably not large because the diets contained only 20% soybean protein.
Animals and diets.
Male Wistar rats (IFFA Credo, l'Arbresle, France) at 5 wk of age, weighing 110 ± 1.7 g were housed in stainless steel cages, maintained at 24°C and at constant humidity (60%) with a 12-h light:dark cycle. The rats received a purified diet (20% casein and 5% sunflower oil) for 10 d. After this adaptation period, they were randomly divided into four groups of five and fed different diets for 2 mo. Two groups received a diet containing 20% purified soybean protein (SOY) [98% purity] or casein (CAS) [95% purity], 10% soybean oil, 7.94% cellulose, 0.29% vitamins, 2.5% minerals, with starch and sucrose to 100% as shown in Table 1. The other groups received the same diets supplemented with 0.1% cholesterol + 0.1% cholic acid + 0.025% choline chlorure (SOY-C and CAS-C). Cholic acid and choline chlorure were added to diets (SOY-C and CAS-C) to improve cholesterol absorption by intestine. We chose 0.1% cholesterol to mimic human cholesterol consumption. Diets and water were freely available. We followed the general guidelines for the care and use of laboratory animals as set forth by the Council of European Communities (1986).
Blood and liver samples.
After completing the 2-mo dietary period, rats were food deprived for 12 h and anesthetized with sodium pentobarbital (60 mg/kg body weight). Blood was collected from the abdominal aorta into tubes containing EDTA, and plasma was prepared by low speed centrifugation (1000 × g for 20 min). Liver was removed from each rat, blotted on filter paper, weighed and divided to prepare microsomes as follows: 2 g to measure HMG-CoA reductase and cholesterol 7 Fecal steroid analysis.
Feces were collected during the last week of the experiment, homogenized, dried and powdered. Bile acids and neutral steroids were separated from feces according to Riottot et al. (1993) Lipid analysis.
Total cholesterol and triacylglycerol concentrations in plasma were determined with Boehringer enzyme kits (Boehringer, Meylan, France) with cholesterol and glycerol as standards, respectively. Liver and microsomal lipids were extracted according to the method of Folch et al. (1957). Liver phospholipid and triacylglycerol fractions were isolated by TLC according to the method of Stahl et al. (1956) Microsomal enzyme activities.
Microsomes for 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase, EC 1.1.1.34) and cholesterol 7 Statistical analysis.
Statistical analysis of the data was conducted by using STATISTICA (Version 4.1, Statsoft, Tulsa, OK). Values are means ± SEM. Data were tested by two-way ANOVA followed by Fisher's least significant difference test. A difference of P < 0.05 was considered significant.
Food consumption, body weight gain, liver weight, relative liver weight and microsomal protein contents.
Body weight gain and food intake did not differ among the four groups after 2 mo of experiment (Table 2). Liver absolute and relative weights did not differ in the SOY and CAS groups but were significantly elevated by cholesterol addition in the rats fed the casein diet. Therefore these variables were lower in the SOY-C group than in the CAS-C group. With or without dietary cholesterol, the hepatic microsomal protein concentration was significantly higher in rats fed soybean protein than in those fed casein (P < 0.001). Cholesterol supplementation of the control diets led to significantly greater microsomal protein concentrations (P < 0.01).
Plasma, liver and liver microsomal lipids.
Neither dietary protein nor cholesterol supplementation affected plasma cholesterol or triacylglycerol concentrations (Table 3). Rats fed SOY and CAS diets did not differ in liver cholesterol or triacylglycerol concentrations, but dietary cholesterol enhanced these liver lipids in rats fed both types of protein. Liver cholesterol and triacylglycerol concentrations were lower in the SOY-C group than in the CAS-C group. Cholesterol level per milligram of liver microsomal protein was lower in the SOY group than in the CAS group and raised by cholesterol supplementation only in the rats fed the soybean protein diet.
Fecal steroid excretion.
Fecal neutral and acidic steroid excretion was higher in the rats fed soybean protein than in those fed casein (Table 4, P < 0.01) and greater in both groups fed the cholesterol-enriched diet, compared with the control groups (P < 0.001).
Hepatic HMG-CoA reductase and cholesterol 7
Desaturase activities.
The
Fatty acid composition of liver microsomal total lipids and hepatic phospholipids.
The percentage of 18:2(n-6) was higher, whereas concomitantly lower percentages of 16:0 and 22:6(n-3) were observed in liver microsomes of the SOY group compared with the CAS group (Table 7). Although no modification was found in the proportions of 20:4(n-6) in the SOY and CAS groups, the 20:4(n-6)/18:2(n-6) ratio, which reflects the overall conversion of 18:2(n-6) to 20:4(n-6) by desaturation-elongation, was lower in the SOY group than in the CAS group. This ratio did not differ in the SOY-C and CAS-C groups.
In this study, no hypocholesterolemic effect of soybean protein compared with casein was observed, a result that is inconsistent with those reported by several studies. We used highly purified soybean protein and have therefore excluded the possible effects of non-protein components such as fiber on intestinal absorption of steroids. Soybean fiber has been shown to exert a moderate hypocholesterolemic effect in rats when ingested in relatively large amounts (Lo et al. 1987
INTRODUCTION
Abstract
Introduction
Methods
Results
Discussion
References
). Soybean protein compared with casein with or without dietary cholesterol (Choi et al. 1989) lowers plasma cholesterol and triacylglycerol concentrations in rats. Several studies have suggested that the hypocholesterolemic effect of vegetable protein, particularly soybean protein, is largely attributable to higher fecal steroid excretion as a consequence of the reduction in intestinal absorption (Nagata et al. 1982). Iwami et al. (1986) reported that soybean protein isolate was inferior to casein in digestibility and suggested that the hydrophobic peptides of soybean protein that remain after digestion bind well to bile acids and serve as a cholesterol-lowering factor. Non-protein components (such as fiber, phytic acid, minerals and isoflavones) associated with soybean protein may also affect cholesterol metabolism (Potter 1995). In compensation for the fecal loss of steroids, soybean protein may stimulate hepatic activities of hydroxy methylglutaryl CoA (HMG-CoA)4 reductase, the rate-limiting enzyme in the biosynthesis of cholesterol (Nagata et al. 1982), and cholesterol 7-hydroxylase, the key enzyme that converts cholesterol to bile acids (Beynen 1990). On the other hand, Saeki and Kiriyama (1990) reported that the difference in the amino acid composition of soybean protein and casein is the main factor affecting plasma cholesterol level. However, no significant differences in cholesterol absorption and excretion were observed between rats fed amino acid mixtures equivalent to both proteins (Nagata et al. 1982). Factors other than the amino acid composition may also be involved in cholesterol metabolism. Moreover, dietary protein can also modify essential fatty acid metabolism (Huang et al. 1993). In rats, soybean protein, compared with casein, reduces 6(n-6) desaturase activity in liver microsomes (Koba et al. 1993). This is the first enzyme responsible for polyunsaturated fatty acid biosynthesis. Similarly, the lower 20:4(n-6)/18:2(n-6) ratio, the linoleate desaturation index, that is observed in liver microsomes of rats fed soybean protein compared with casein-fed rats has also been attributed to reduced 6(n-6) desaturase activity (Choi et al. 1989).
-hydroxylase activities) and fatty acid biosynthesis. The desaturase activities studied were 6 desaturase [with 18:2(n-6) or 18:3(n-3) as substrate] and 5 desaturase [with 20:3(n-6) as substrate]. Additionally, the fatty acid compositions of liver phospholipids and hepatic microsomal total lipids were determined to see whether the modifications in desaturation rates measured in vitro were reflected in the fatty acid profile.
MATERIALS AND METHODS
Abstract
Introduction
Methods
Results
Discussion
References
View this table:
Table 1.
Compositions of experimental diets1
-hydroxylase activities; 3.5 g for desaturation assays; and 1 g for lipid analysis. The same lobe of each rat's liver was used for a particular assay.
-linolenic acid 8, 11, 14) (1.7 GBq/mmol) were obtained from NEN (Les Ulis, France). DL-HMG-CoA, cholesterol, biliary acids and neutral steroids were obtained from Sigma-Aldrich (l'Isle d'Abeau, France). Fatty acids (linoleic, -linolenic, -linolenic, stearidonic, dihomo--linolenic and arachidonic acids) were provided by Nu-Chek-Prep. Other chemicals were reagent grades from standard commercial sources.
. Bile acids were deconjugated by the method of Grundy et al. (1965). Neutral steroid and bile acid samples were then derivatized by using a mixture of BSTFA/Deriva-sil/dichloromethane (40:10:50 v/v/v). Measurements were carried out by GLC (see above).
. Phospholipids were estimated by their phosphorus content using Bartlett's method (1959). Fatty acid compositions of microsomal lipids and total liver phospholipids were analyzed by GLC (see above). Liver and hepatic microsomal cholesterol levels were measured according to the method of Gambert et al. (1979) by using GLC (see above). The protein content of microsomes was measured according to Layne (1957).
-hydroxylase (EC 1.14.13.17) were prepared from liver as described by Al-Shubaji et al. (1991). The activity of HMG-CoA reductase was measured on liver microsomes with 3-[14C] HMG-CoA as substrate. Labeled mevanolactone was separated from unreacted HMG-CoA by column chromatography containing AG1-X8 resin (formate 200-400, analytical grade, Biorad, France) (Wilce and Kroon 1992). HMG-CoA reductase activity was expressed as pmol of 3-[14C]HMG-CoA transformed into [14C]mevanolactone/(min·mg microsomal protein), after correcting for recovery of [3H]mevanolactone from the column. The activity of cholesterol 7-hydroxylase was measured as described by Jelinek et al. (1990) with hydroxycholesterol as internal standard. Cholesterol 7-hydroxylase activity was expressed as pmol of [14C] cholesterol transformed into [14C]hydroxycholesterol/(min·mg microsomal protein). Desaturase activities were assayed exactly as previously reported (Cao et al. 1995). Microsomes were incubated with a low or saturating level of substrate, 60 or 120 nmol of [1-14C] linoleic acid for 6(n-6) desaturation, 60 or 120 nmol of [1-14C] -linolenic acid for 6(n-3) desaturation and 40 or 80 nmol of [1-14C] dihomo--linolenic acid for 5(n-6) desaturation. The conversion of the three labeled substrates into their corresponding products (-linolenic, stearidonic and arachidonic acid, respectively) was determined after separation by HPLC (as described above). Desaturation rates are expressed as nmol of desaturation products/(15 min·5 mg microsomal protein).
RESULTS
Abstract
Introduction
Methods
Results
Discussion
References
View this table:
Table 2.
Food intake, body weight gain, liver weight and liver microsomal protein concentration of rats fed soybean protein or casein diets supplemented or not with cholesterol1,2
View this table:
Table 3.
Plasma, liver and liver microsomal lipids of rats fed soybean protein or casein diets supplemented or not with cholesterol1,2
View this table:
Table 4.
Fecal steroid excretion by rats fed soybean protein or casein diets supplemented or not with cholesterol1,2
-hydroxylase activities.
The HMG-CoA reductase activity was 1.7-fold higher in the SOY group than in the CAS group, but the difference was not significant due to large individual variation (Table 5). Dietary cholesterol supplementation lowered HMG-CoA reductase activity; the difference between the soy group and the SOY-C group (
86%) was significant, whereas the 46% lower value in CAS-C fed rats compared with those fed CAS was not significantly different.
View this table:
Table 5.
HMG-CoA reductase and cholesterol 7 -hydroxylase activities of rats fed soybean protein or casein diets supplemented or not with cholesterol1,2,3
-hydroxylase activity was diminished (30%) in the SOY group compared with the CAS group. Cholesterol addition lowered this activity only in the rats fed the casein diet, so much so that cholesterol 7-hydroxylase activity was 60% higher in the SOY-C group than in the CAS-C group (P < 0.05, Table 5).
6(n-6) desaturation rate, with both substrate levels (60 and 120 nmol) was lower in the SOY group than in the CAS group (20 and 34%, respectively) and was higher (+33 and +19%, respectively) in the SOY-C group than in the CAS-C group. Cholesterol supplementation lowered this activity only in rats fed the casein diet.
6(n-3) desaturation rate, at low substrate level (60 nmol), was lower in the SOY group than in the CAS group (Table 6). However, at a high substrate level (120 nmol), the desaturation rate was not affected by dietary protein. The 6(n-3) desaturation rate, with 120 nmol of substrate, was significantly lowered by cholesterol supplementation (27% in the casein-fed rats and 18% in the rats fed soybean protein), compared with the corresponding groups fed diets without cholesterol.
View this table:
Table 6.
Microsomal desaturase activities of rats fed soybean protein or casein diets supplemented or not with cholesterol1,2
5 desaturation did not differ in the rats fed soybean protein and those fed casein, for both substrate concentrations (Table 6). Supplementation with cholesterol markedly diminished 5(n-6) desaturation rate (nearly 60%) in rats fed both proteins (P < 0.001).
View this table:
Table 7.
Fatty acid composition of microsomal total lipids of rats fed soybean protein or casein diets
supplemented or not with cholesterol1,2
View this table:
Table 8.
Fatty acid composition of liver phospholipids of rats fed soybean protein or casein diets supplemented or not with cholesterol1,2
DISCUSSION
Abstract
Introduction
Methods
Results
Discussion
References
). In humans, Bakhit et al. (1994) reported that consuming soybean protein with soybean fiber lowers plasma and LDL cholesterol in hypercholesterolemic subjects. Isoflavones from soybean have also been hypothesized as the cause of the cholesterol-lowering effect. Anthony et al. (1996) showed that the isoflavone-intact protein, but not the alcohol-extracted soybean protein reduced plasma cholesterol in peripubertal rhesus monkeys. Because we did not use aqueous alcohol extraction for soybean protein, the purified soybean protein used in our study might still contain isoflavones in low quantity; however, feeding rats these proteins did not produce any hypocholesterolemic effect in comparison with casein (Table 1). The mechanism is likely to vary, depending on the animal model, and the responsible component may react differently, depending on the species. Furthermore, Nagata et al. (1982), observed the hypocholesterolemic effect in rats fed the soybean protein-type amino acid vs. the casein-type mixture. The effect was attributed to the depression of hepatic cholesterol synthesis because the rates of cholesterol absorption and excretion were similar with both mixtures. Hence, the difference in the amino acid compositions of the proteins was considered to be the main factor involved in their differential action on plasma cholesterol. When intact proteins were fed (Nagata et al. 1982), the decreased intestinal absorption of cholesterol and increased fecal steroid excretion were responsible for the hypocholesterolemic effect of soybean protein compared with casein. In this way, soybean protein, compared with casein, stimulated hepatic cholesterol synthesis in response to increased fecal steroid excretion (Nagata et al. 1982). The undigested components of soybean protein are likely to inhibit the plasma cholesterol-lowering effect observed with the amino acid mixture simulating soybean protein. In this study, highly purified soybean protein, with or without dietary cholesterol, compared with casein, raised the fecal excretion of bile acids and neutral steroids (Table 4), suggesting a possible effect of hydrophobic peptides. These peptides strongly interfere with steroid intestinal absorption and enhance steroid excretion in feces as previously reported (Iwami et al. 1986, Sugano et al. 1990). However, the increased excretion of fecal steroids (Table 4) was not associated with a lower plasma cholesterol level (Table 2), a finding that is inconsistent with those previously reported. In our study, we probably minimized fecal steroid excretion by using highly purified soybean protein, which might be responsible for the absence of the cholesterol-lowering effect of soybean protein compared with casein. Moreover, HMG-CoA reductase activity, which tended to be higher in the rats fed the cholesterol-free highly purified soybean protein diet than in those fed casein (Table 5), may compensate for the loss of fecal steroids without modifying plasma cholesterol concentration.
showed that rats fed soybean protein rather than casein had higher hepatic cholesterol 7-hydroxylase activity. In this study, cholesterol 7-hydroxylase activity was higher in rats fed the highly purified soybean protein diet compared with those fed casein but only in the presence of 0.1% cholesterol. In the absence of dietary cholesterol, highly purified soybean protein lowered cholesterol 7-hydroxylase activity (Table 5). This was associated with higher bile steroid excretion (Table 4). However, Choi et al. (1989) showed no dietary protein-dependent difference in cholesterol 7-hydroxylase activity among rats fed soybean protein or casein supplemented or not with cholesterol.
). These authors reported that the hypocholesterolemic effect of soybean protein compared with casein, as well as the hypercholesterolemic effect of exogenous cholesterol was observed when rats were fed a higher level (
0.25% cholesterol). But these amounts are higher than the quantities consumed by humans (usually <0.05%).
, Raheja and Linscheer 1982). Lee et al. (1991) obtained similar results, showing that dietary cholesterol (0.05-1.0 g/100 g) did not greatly influence the concentration of serum cholesterol, but markedly increased liver cholesterol in a dose-dependent manner. HMG-CoA reductase activity was lowered by cholesterol supplementation, and this decrease was more marked in rats fed the soybean protein diet (Table 5). Similar findings were reported by Choi et al. (1989). This was probably due to greater hepatic cholesterol levels, which exert an inhibitory feedback effect on endogenous synthesis of cholesterol as previously suggested (Wilce and Kroon 1992).
-hydroxylase was diminished by cholesterol supplementation in the rats fed casein, but not modified in those fed soybean protein. Bosisio et al. (1981) showed an induction of cholesterol 7-hydroxylase activity in rats fed cholesterol-supplemented diets vs. unsupplemented diets. In this study, exogenous cholesterol did not stimulate bile acid synthesis, but dietary cholic acid, which was carried by cholesterol, may have exerted a negative feedback regulation on cholesterol 7-hydroxylase activity. Indeed, Shefer et al. (1973) reported that diets supplemented with bile acids diminish de novo synthesis of bile acids and secretion of bile acids into bile.
6(n-6) desaturation rate (Table 6) as previously observed (Choi et al. 1989, Koba et al. 1993). Soybean protein reduced 6(n-3) desaturation (Table 6) only at the low substrate level (60 nmol). The differential response of both desaturases with 120 nmol of substrate supports the hypothesis for the existence of two different desaturation enzymes as previously suggested (Cao et al. 1995). 5(n-6) Desaturation (Table 6) was not modified by either dietary protein, and this result is in agreement with that of Koba et al. (1993) who reported that dietary protein modulates desaturase activities through its effect on membrane fluidity. In liver microsomes, soybean protein, compared with casein, lowered the cholesterol level and the cholesterol/phospholipid ratio, raised membrane fluidity and subsequently reduced 6 desaturase. Data in Table 6 are consistent with the results of Koba et al. (1993) because 6(n-6) and probably 6(n-3) desaturase activities in rats fed cholesterol-free diets were related to microsomal cholesterol contents (Table 3). When diets were enriched in cholesterol, 6(n-6) desaturation, at the two substrate levels, was higher in rats fed soybean protein than in those fed casein (Table 6). This result is inconsistent with that reported by Lindholm and Enklund (1991). The difference in the response in 6(n-6) desaturase activity to dietary protein enriched in cholesterol may be attributable to differences in the experimental conditions because these latter authors used 0.5% dietary cholesterol and a low substrate [18:2(n-6)] level for 6(n-6) desaturase assay.
5 desaturation was affected to a greater extent than 6(n-6) and 6(n-3) desaturations, whatever the dietary protein. A similar finding was reported by Leikin and Brenner (1987). Like HMG-CoA reductase, 5(n-6) desaturase activity also appeared particularly sensitive to hepatic cholesterol contents. Finally, dietary cholesterol diminished overall desaturation in both protein-fed groups. This suggests a primary role for cholesterol, rather than for dietary protein quality, in the regulation of linoleate and linolenate metabolisms with 5 desaturation being more sensitive than 6 desaturation. Brenner (1990) also showed that dietary cholesterol decreases 6(n-6) and 5(n-6) desaturase activities associated with a decrease in membrane fluidity and an increase in the phosphatidylcholine/phosphatidylethanolamine ratio in rat liver microsomes. With regard to these results, Brenner (1990) suggested that changes in the phospholipids due to ingested cholesterol may decrease 6(n-6) and 5(n-6) desaturase activities.
6(n-6) desaturation. Our findings confirm the suggestion of Ogawa et al. (1992) that the conversion of linoleic acid to arachidonic acid was lower in rats fed soybean protein than in those fed casein. Cholesterol-free soybean protein also lowered the 22:6(n-3) level, suggesting a decreased conversion of 18:3(n-3) to 22:6(n-3), in agreement with the results reported previously (Noguchi et al. 1992). All of these effects, however, disappeared in liver microsomal total lipids as well as in hepatic phospholipids when diets were cholesterol enriched (Tables 7 and 8).
. Indeed, Tables 7 and 8 indicate clearly that cholesterol supplementation increased 18:2(n-6) and decreased 20:4(n-6) contents in liver microsomal lipids and hepatic phospholipids. The 18:1(n-9)/18:0 ratio increased with dietary cholesterol regardless of the dietary protein (Tables 7 and 8), suggesting higher 9 desaturase activity. A similar finding was previously reported (Leikin and Brenner 1987).
-hydroxylase activities were greatly affected.
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FOOTNOTES |
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Manuscript received 28 May 1997. Initial reviews completed 23 June 1997. Revision accepted 16 March 1998.
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LITERATURE CITED |
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Abstract
Introduction
Methods
Results
Discussion
References
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-hydroxylase, the rate-limiting enzyme in bile acid biosynthesis.
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265:8190-81976 desaturase activity of rat hepatic microsomes.
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26:107-110[Medline] -linolenic acid metabolism in rats.
J. Nutr. Sci. Vitaminol.
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38:579-591 
-cyclodextrin in the hamster and in the genetically hypercholesterolemic Rico rat.
Lipids
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28:181-188[Medline] -hydroxylase in the rat.
J. Lipid Res.
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