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Journal of the American College of Nutrition, Vol. 19, No. 5, 601-607 (2000)
Published by the American College of Nutrition

Original Research

Comparative Cholesterol Lowering Properties of Vegetable Oils: Beyond Fatty Acids

Thomas A. Wilson, PhD, MPH, Lynne M. Ausman, DSc, Carl W. Lawton, PhD, D. Mark Hegsted, PhD and Robert J. Nicolosi, PhD

Department of Health and Clinical Science (T.A.W, R.J.N.), Center for Chronic Disease Control and Prevention, University of Massachusetts
Department of Chemical Engineering (C.W.L.), Center for Chronic Disease Control and Prevention, University of Massachusetts
Lowell, Human Nutrition Research Center on Aging, Boston, and School of Nutrition, Medford, Tufts University (L.M.A.), Massachusetts
Harvard Medical School, New England Regional Primate Research Center, Southboro (D.M.H.), Massachusetts

Address reprint requests to: Dr. Robert J. Nicolosi, Director, Center for Chronic Disease Control and Prevention, Department of Health & Clinical Sciences, 3 Solomont Way, Suite 4, University of Massachusetts Lowell, Lowell, MA 01854-5125. E-mail: Robert_Nicolosi{at}uml.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Objective: Our laboratory has previously reported that the hypolipidemic effect of rice bran oil (RBO) is not entirely explained by its fatty acid composition. Although RBO has up to three times more serum cholesterol-raising saturated fatty acids (SATS) than some unsaturated vegetable oils, we hypothesized that its greater content of the unsaponifiables would compensate for its high SATS and yield comparable cholesterol-lowering properties to other vegetable oils with less SATS.

Methods: To study the comparative effects of different unsaturated vegetable oils on serum lipoprotein levels, nine cynomologus monkeys (Macaca fascicularis) were fed diets, for four weeks, in a Latin square design, containing rice bran, canola or corn oils (as 20% of energy) in a basal mixture of other fats to yield a final dietary fat concentration of 30% of energy. All animals were fed a baseline diet containing 36% of energy as fat with 15% SATS, 15% monounsaturated fatty acids (MONOS) and 6% polyunsaturated fatty acids (POLYS).

Results: Despite the lower SATS and higher MONOS content of canola oil and the higher POLYS content of corn oil, RBO produced similar reductions in serum total cholesterol (TC) (-25%) and low density lipoprotein cholesterol (LDL-C) (-30%). In addition, as compared to the baseline diet, the reduction in serum TC and LDL-C cholesterol with RBO was not accompanied by reductions in high density lipoprotein cholesterol (HDL-C) which occurred with the other two dietary oils. Using predictive equations developed from data gathered from several studies with non-human primates, we noted that the observed serum TC and LDL-C lowering capabilities of the RBO diet were in excess of those predicted based on the fatty acid composition of RBO.

Conclusions: These studies suggest that non-fatty acid components (unsaponifiables) of RBO can contribute significantly to its cholesterol-lowering capability.

Key words: rice bran oil, unsaponifiables, hypercholesterolemic, saturated fat, monounsaturated fat, polyunsaturated fat


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
There have been numerous studies in humans and animals that have demonstrated that oils containing saturated fatty acids (SATS) raise serum total cholesterol (TC) and, in particular, low density lipoprotein cholesterol (LDL-C) levels [1–3], while those enriched in unsaturated fatty acids [1–9] lower LDL-C when replacing saturated fat. In general, the predictive equations of Keys et al. [2] and Hegsted et al. [3] have demonstrated that the fatty acid components and cholesterol in the diet are the primary determinants of diet induced hypo- or hypercholesterolemia. However, a review of several studies has also indicated a hypocholesterolemic effect of some unsaponifiables, in particular, plant sterol components [10]. Several investigators have reported that not only can plant sterols significantly lower LDL-C levels, even at relatively low intakes [11–16], but also that some plant sterols are more active than others [14–16]. In addition, cholesterol-lowering effects of other unsaponifiables such as tocotrienols, an analog of tocopherol found in rich concentrations in palm oil [17–21], and oryzanol, a ferulic acid ester of phytosterols and tritrepene alcohols found in soybean oil [22–26], have been reported.

Particularly germane to the studies reported in this communication is the finding that crude rice bran oil (CRBO) contains an unusually high content of unsaponifiables (up to 4.4%), at a level which is several times greater than most other vegetable oils. The unsaponifiables of CRBO are composed of plant sterols (43%), 4-methyl sterols (10%), triterpene alcohols (29%) and less polar components such as squalene or tocotrienols (19%). In addition, RBO contains up to 20% saturated fatty acids and approximately equal amounts of polyunsaturated (40%) and monounsaturated fatty acids (40%), a fatty acid profile quite different from other often-utilized hypocholesterolemic vegetable oils. In recently reported studies, the hypocholesterolemic action of RBO has been attributed to its yet poorly characterized unsaponifiables. For example, studies in rats [27,28] have shown that the unsaponifiables of RBO lowered serum TC and LDL-C and raised high-density lipoprotein cholesterol (HDL-C) and that these alterations in lipoprotein cholesterol were associated with increased fecal excretion of neutral sterols and total bile acids. Our first study in monkeys confirmed the LDL-C and apo B-lowering properties of RBO and suggested that the fatty acid composition of RBO did not entirely explain its cholesterol-lowering properties [29]. One study in humans fed 35 to 40 grams of either RBO or some combination of coconut oil, palm oil or ground nut oil showed 25% to 30% reductions in serum TC levels in the RBO group [30]. However, this study needs to be qualified because of the highly SATS nature of tropical oils and the limited information on ground nut oil. A report of a human trial of RBO [31] compared to other vegetable oils designed in a manner similar to the current monkey study also demonstrated significant serum LDL-C lowering properties of RBO which were not entirely explained by the predictive equations of either Keys et al. [2] or Hegsted et al. [3] based on the fatty acid composition of RBO. Thus the reports in the literature combined with the results of the present communication suggest a significant contribution of the unsaponifiable fraction of RBO to its cholesterol-lowering properties.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Diet and Experimental Protocol
Nine adult male cynomolgus monkeys (Macaca fascicularis) between the ages of five and eight years were fed a baseline diet in which the fat level and composition represented the "Average American Diet" (AAD) - 36% of energy as fat with 15% saturated fatty acids (SATS), 15% monounsaturated fatty acids (MONOS) and 6% polyunsaturated fatty acids (POLYS) and a variety of experimental diets. These experimental diets contained rice bran, canola and corn oils (as 20% of energy) to which a mixture of other fats were added to bring the final dietary fat concentration to 30% of energy. The monkeys were fed the vegetable oil diets for a 28-day period in a Latin square design to minimize any order effects. The composition of the diets is given in Table 1 and the fatty acid composition of the oil blends in Table 2. Animals were maintained in accordance with the guidelines of the Committee of Animals of the University of Massachusetts Lowell Research Foundation, and the guidelines were prepared by the Committee on Care in Use of Lab Animals of the Institute of Lab Animal Resources, National Research Council (DHEW Publication No. 85-23, Revised 1985). All food and water were available ad libitum.


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  		Table 1. Composition of purified monkey diets (g/kg)a

 

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  		Table 2. Fatty acid composition of experimental dietary oil blends (g/100 g)

 
Sample Collection and Analyses
After an overnight fast, monkeys were tranquilized with Ketamine (Bristol Laboratories, Veterinary Products, Syracuse, NY), and blood samples were drawn from the femoral vein into tubes containing no anticoagulant. After allowing the samples to clot, serum was separated at 2500 rpm for 20 minutes at 4°C, and 0.2 mM phenylmethysulfonyl fluoride and N-ethylmaleimide (0.125%, Sigma Chemical Co., St. Louis, MO) were added as proteolytic and lecithin: cholesterol acyltransferase (LCAT) inhibitors, respectively. Serum TC [32] and triglycerides (TG) [33] were quantified using enzymatic methods which we have previously described [29]. HDL-C was estimated after heparin-Mn2+ precipitation [34] of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). The LDL-C fraction (very low density (VLDL-C) and low density lipoprotein cholesterol) was determined by the difference between TC and HDL-C. Assays were standardized by participation in the Centers for Disease Control - National Heart, Lung and Blood Institute Standardization Program. Values for serum TC, LDL-C, HDL-C, and TG were derived from blood samples taken on the 24th and 28th day of the study. The unsaponifiable fraction of RBO was measured as described by Rogers et al. [35].

Statistics
The PROC GLM procedure of Statistical Analysis System (SAS-PC) was utilized to analyze the data with a two-way analysis of variance for repeated measures with monkey and diet as the main effects. When the analysis of variance showed a significant main effect, Tukey’s t test at the p < 0.05 level was carried out to compare means. To normalize the data and to stabilize the variance, the raw data were transformed to log10 values before any analyses were performed [36].

Equations to predict the serum TC and LDL-C response of the Macaca fascicularis monkeys to changes in dietary SATS, MONOS and POLYS and dietary cholesterol have been developed (Ausman et al., unpublished data) according to the approach of Hegsted et al. [3] with some modification. Data from 454 experimental periods (one experimental period is defined as one monkey fed one diet) derived from 56 monkeys fed up to 29 different diets were classified according to study (18 studies over the past few years). A study is defined as a group of monkeys containing individuals each consuming a set group of diets (from two up to ten diets). A study group traditionally contains from six to ten animals. An analysis of covariance with study as the covariate and the dietary SATS, MONOS and POLYS and dietary cholesterol as the main variables was carried out to examine the response of the serum TC and LDL-C to the imposed diet. The resulting regression equation without the covariate term and with the coefficients for the dietary variables can be used to predict the change in serum TC or LDL-C in response to the change in dietary components. All 29 diets included in these analyses were semipurified and had a similar composition except for amount and type of fat and amount of dietary cholesterol. Furthermore, the range of serum TC (100–800 mg/dL) responses to the imposed diets was much greater than for humans [2,3], and each individual monkey appeared to vary around a different set-point. Therefore, the analysis was further refined to make two regression equations - one for monkeys whose serum TC was less than 300 mg/dL on a diet approximating the fat composition of the AAD (low) and another for monkeys with serum TC levels >= 300 mg/dL on this same diet (high).

The change ({Delta}) equations developed for the low monkeys are (n=106 values):

((Eq. 1))

((Eq. 2))
where S, P and M are the SATS, POLYS and MONOS content of the diet (as % of energy) and C is the cholesterol content of the diet (mg/418.4 kJ).

The change ({Delta}) equations developed for the high monkeys are (n = 101 values):

((Eq. 3))

((Eq. 4))

The R2D value is the percent of the non-animal variance accounted for by the dietary variables. In all cases, the coefficient for P was not significant and the coefficients for S, M and C were significant at p < 0.01. The overall significance of each of the models was p < 0.0001. These change equations can be used to predict the response of each of the nine monkeys in the current study to the defined dietary changes when switched from the AAD to each of the canola, corn and rice bran oil diets.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Table 3 represents the serum lipid concentrations for the monkeys for each of the four diets from baseline to four weeks of dietary treatment. However, because the data were highly skewed, the statistical comparisons were carried out on log10 values. For all diets, serum TC and LDL-C decreased significantly from baseline. While serum HDL-C levels decreased significantly when monkeys were fed the canola oil diet, they showed no change from baseline when fed the RBO based diet. Serum HDL-C concentrations in the corn oil fed group appeared to decrease although this change was not significantly different from baseline. Serum TG levels were reduced compared to baseline in all treatment diets although only significantly in the monkeys fed the corn oil diet.


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  		Table 3. Plasma lipid lipoprotein and TG concentrations (mg/dL) in monkeys after four weeks of dietary treatment

 
To compare the performance of the experimental diets to each other, the change of each diet from baseline was utilized as the analyzed variable (Table 4). Again, the statistical analysis was done with log10 values. In this case, there were no significant differences in the response of the rice bran, canola, and corn oil fed monkeys for serum TC, LDL-C and TG. The reductions of serum HDL-C in the canola and corn oil fed monkeys were greater than for the RBO fed monkeys.


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  		Table 4. Change from AAD, using log10 transformed values for serum TC, LDL-C, HDL-C and TG

 
The changes in serum TC and LDL-C when the monkeys were switched from the AAD to each of the experimental vegetable oils can be compared to predicted changes based on our knowledge of the fatty acid contents of the diets and their effects on circulating lipids using Eq. 1–4. In this study, four monkeys were classified in the low group (Eq. 1 & 2 ) and five in the high group ( Eq. 3 & 4). The predicted changes for the monkeys, as well as the observed changes, are given in Tables 5 and 6. It is noteworthy that the predicted and observed changes for the canola and corn oil groups were similar. However, monkeys fed the RBO diet consistently performed better than expected.


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  		Table 5. Change in serum TC concentration (mg/dL) from AAD to a 30% fat diet with 20% energy from vegetable oil for all monkeys (Mean ± SD)

 

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  		Table 6. Change in serum LDL-C concentration (mg/dL) from AAD to a 30% fat diet with 20% energy from vegetable oil for all monkeys

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
There are abundant data available from studies with human subjects [1–7], non-human primates [37,38] and appropriate rodent species [39,40] that demonstrate the primary effects of SATS and dietary cholesterol upon the circulating levels of lipoproteins. In this study, the RBO containing diet had 35% more SATS and 29% less MONOS than canola oil and 33% less POLYS (linoleic acid) than corn oil, and yet the reductions in serum LDL-C levels were comparable to those of the other two vegetable oils as compared to the baseline diet. Thus, the results of this study can only be explained by assuming that there is something unique about the composition of RBO which, under these conditions, dominates the results and obscures the effects of the fatty acid components which were modified in the diets. Previous studies have indicated that the unsaponifiable component of RBO, i.e., the plant sterols and oryzanol, are the major cholesterol-lowering factors in RBO [22–26]. A recent study published by our laboratory in hamsters demonstrated that the reductions in serum LDL-C levels with oryzanol feeding were associated with similar decreases in aortic fatty streak formation [41]. In addition RBO also contains tocotrienols, reported to inhibit cholesterol synthesis [17–21]. Analysis of the refined RBO used in the current study revealed concentrations of plant sterols, oryzanol and tocotrienols of 11130, 720 and 300 ppm, respectively. Plant sterols were found at levels 50% to 70% lower in the corn and canola oils, and the oryzanol and tocotrienols were not detected in either of these oils. Thus, it is impossible to state with any certainty which unsaponifiable component or a combination of all three is the contributing component to the hypocholesterolemic response of RBO in the present study.

In order to compare the observed responses of the monkeys to those expected based on fatty acid content alone, multiple regression equations were utilized (Eq. 1–4). These equations indicate that the absolute response of these monkeys to dietary fatty acid and cholesterol change varies from that of humans [2,3], with a subset of the monkeys being much more responsive to dietary SATS and cholesterol. However, unlike the human data, which shows that SATS is more hypercholesterolemic fat, followed by MONOS and then by POLYS, the present study shows no difference in dietary fat saturation and plasma cholesterol concentrations. The RBO, higher in SATS, the canola oil, higher in MONOS, and the corn oil, higher in POLYS, all produced a similar hypocholesterolemic response in the monkeys. Also, when applied to the average serum lipid values generated from this experiment (Tables 5 and 6), the greatest error in prediction appeared in the RBO group, which is consistent with the hypothesis that dietary components other than fatty acids may be playing a role.

A similar study carried out in humans [31] in which RBO was compared to other vegetable oils as part of the AHA Step II diet also showed the cholesterol-lowering property of RBO, which was observed in the present study in monkeys fed a diet resembling the AHA Step I diet. However, in the human study [31], plasma HDL-C was decreased with the consumption of RBO, thereby not improving the TC/HDL-C ratio, a circumstance which was not the case in the present monkey study. In the monkeys, the canola oil diet significantly reduced HDL-C from baseline, whereas the RBO did not. Also, the 20% reduction in serum LDL-C levels in humans fed RBO was virtually identical to that predicted from our earlier reported study in monkeys [29]. The human subjects were fed diets with a fat composition similar to that of the "Average American Diet," and then diets with each of the four vegetable oils showed that the hypocholesterolemic response of RBO was greater than predicted.

In conclusion, despite the less than optimal fatty acid composition of RBO as compared to the other unsaturated vegetable oils, studies in both humans and monkeys show that reductions in serum LDL-C levels with RBO feeding were greater than expected, suggesting an important contribution of the non-fatty acid fraction of RBO to its cholesterol-lowering properties. Also, RBO compared with other vegetable oils does not reduce serum HDL-C, thereby decreasing the TC/HDL-C ratio.


   ACKNOWLEDGMENTS
 
This work was supported in part by NIH grant RO1HL39385. The authors thank Donato Vespa, Lorraine Misner and Subbiah Yoganathan for technical assistance.

Received June 19, 1998. Accepted July 6, 2000.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. The Expert Panel: Report of the National Cholesterol Education Program Panel on detection, evaluation, and treatment of high blood cholesterol in adults. Arch Intern Med 148: 36–64, 1988.[Abstract]
  2. Keys A, Anderson JT, Grande R: Prediction of serum cholesterol responses of man to changes in fats in the diet. Lancet 2: 959, 1957.
  3. Hegsted DM, McGandy RB, Myers ML, Stare FJ: Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr 17: 281–295, 1965.[Medline]
  4. Mattson FH, Grundy SM: Comparison of effects of dietary saturated, monounsaturated, and poly-unsaturated fatty acids on plasma lipids and lipoproteins in man. J Lipid Res 26: 194–202, 1985.[Abstract]
  5. Mensink RP, Katan MB: Effect of a diet enriched with monounsaturated or polyunsaturated fatty acids on levels of low-density and high-density lipoprotein cholesterol in healthy women and men. N Engl J Med 321: 436–441, 1989.[Abstract]
  6. McDonald BE, Gerrard JM, Bruce VM, Corner EJ: Comparison of the effect of canola oil and sunflower oil on plasma lipids and lipoproteins and on in vivo thromboxane A2 and prostacyclin production in healthy young men. Am J Clin Nutr 50: 1382–1388, 1989.[Abstract/Free Full Text]
  7. Dreon DM, Vranizan KM, Drauss RM, Austin MA, Wood PD: The effects of polyunsaturated fat vs. monounsaturated fat on plasma lipoproteins. JAMA 263: 2462–2466, 1990.[Abstract]
  8. Brousseau ME, Stucchi AF, Vespa DB, Schaefer EJ, Nicolosi RJ: A diet enriched in monounsaturated fats decreases low density lipoprotein concentrations in cynomolgus monkeys by a different mechanism than does a diet enriched in polyunsaturated fats. J Nutr 123: 2049–2058, 1993.
  9. Brousseau ME, Stucchi AF, Vespa DB, Schaefer EJ, Nicolosi RJ: Diets enriched in unsaturated fatty acids enhance apolipoprotein A-1 catabolism but do not affect either its production or hepatic mRNA abundance in cynomolgus monkeys. Atherosclerosis 115: 107–119, 1995.[Medline]
  10. Pollak OJ, Kritchevsky D: Sitosterol. In Clarkson TB, Kritchevsky D, Pollak OJ (eds): "Monographs on Atherosclerosis." New York: Karger, pp 1–215, 1981.
  11. Grundy SM, Mok HYI: Determination of cholesterol absorption in man. J Lipid Res 18: 263–271, 1977.[Abstract]
  12. Lees AM, Mok HYI, Lees RS, McCluskey MA: Plant sterols as cholesterol-lowering agents: Clinical trials in patients with hypercholesterolemia and studies of sterol balance. Atherosclerosis 28: 325–338, 1977.[Medline]
  13. Heinemann T, Leiss O, vonBergmann K: Effect of low dose sitostanol on serum cholesterol in patients with hypercholesterolemia. Atherosclerosis 61: 219–223, 1986.[Medline]
  14. Best MM, Duncan CH, Van Loon EJ, Walthen JD: Lowering of serum cholesterol by the administration of a plant sterol. Circulation 10: 201–206, 1954.[Medline]
  15. Hassan AS, Rampone AJ: Intestinal absorption and lymphatic transport of cholesterol and ß-sitostanol in the rat. J Lipid Res 20: 646–653, 1979.[Abstract]
  16. Chandler RF, Hooper SN, Ismail HA: Anti-hypercholesterolemic studies with sterols: ß-sitosterol and stigmasterol. J Pharmac Sci 68: 245–247, 1979.[Medline]
  17. Qureshi AA, Qureshi N, Wright JJK, Shen Z, Kramer A, Gapor A, Chong YH, DeWitt G, Ong ASH, Peterson DM, Bradlow BA: Lowering of serum cholesterol in hypercholesterolemic humans by tocotrienols (palmvitee). Am J Clin Nutr 53: 1021S–1026S, 1991.[Abstract/Free Full Text]
  18. Qureshi AA, Burger WC, Elson CE, Peterson DM: The structure of an inhibitor of cholesterol biosynthesis isolated from barley. J Biol Chem 261: 10544–10550, 1986.[Abstract/Free Full Text]
  19. Qureshi AA, Crenshaw TD, Abuirmeileh N, Peterson DM, Elson CE: Impact of minor plant constituents on porcine hepatic lipid metabolism. Atherosclerosis 64: 109–114, 1987.[Medline]
  20. Qureshi AA, Burger NC, Elson CD, Peterson DM: Effects of cereals and culture fitrate of trichoderma viride on lipid metabolism in swine. Lipids 17: 924–928, 1982.[Medline]
  21. Qureshi AA, Qureshi N, Hasler-Rapacz J, Weber FE, Chaudhary V, Crenshaw TD, Gapor A, Ong ASH, Chong YH, Peterson DM, Rapacz J: Dietary tocotrienols reduce concentrations of plasma cholesterol, apolipoprotein B, thromboxane B2, and platelet factor 4 in pigs with inherited hyperlipidemias. Am J Clin Nutr 53: 1042S–1046S, 1991.[Abstract/Free Full Text]
  22. Kiribuchi M, Miura K, Tokuda S, Kaneda T: Hypercholesterolemic effect of triterpene alcohols with soysterol on plasma cholesterol in rats. J Nutr Sci Vitaminol 29: 35–43, 1983.
  23. Sakamoto K, Tabata T, Shirasaki K, Inagaki T, Nakayama S: Effects of gamma-oryzanol and cycloartenol ferulic acid ester on cholesterol diet induced hyperlipidemia in rats. Japan J Pharmacol 45: 559–565, 1987.
  24. Yoshino G, Kazumi T, Amano M, Takiewa M, Yamasaki T, Takashima S, Iwai M, Hatanaka H, Baba S: Effects of gamma-oryzanol and probucol on hyperlipidemia. Current Therap Res 45: 975–982, 1989.
  25. Sasaki J, Takada Y, Kusuda M, Tanabe Y, Matsunaga A, Arakawa K: Effects of gamma-oryzanol on serum lipids and apolipoproteins in dyslipidemic schizophrenics receiving major tranquilizers. Clin Therap 12: 263–268, 1990.[Medline]
  26. Shinomiya M, Morisaki N, Matsuoka N, Izumi Y, Saito A, Kumagai A, Mitani K, Morita S: Effects of gamma-oryzanol on lipid metabolism in rats fed high-cholesterol diet. Tohoku J Exp Med 141: 191–197, 1983.
  27. Sharma RD, Rukmini C. Rice bran oil and hypocholesterolemia in rats. Lipids 21: 715–717, 1986.[Medline]
  28. Seetharamaiah GS, Chandrasekhara N: Studies on hypocholesterolemic activity of rice bran oil. Atherosclerosis 78: 219–223, 1989.[Medline]
  29. Nicolosi RJ, Ausman LM, Hegsted DM: Rice bran oil lowers serum total and low density lipoprotein cholesterol and Apo B levels in nonhuman primates. Atherosclerosis 88: 133–142, 1991.[Medline]
  30. Raghuram TC, Brahmaji TC, Rukmini C: Studies on the hypolipidemic effects of dietary rice bran oil in human subjects. Nutr Rep Int 39: 889–895, 1989.
  31. Lichtenstein AH, Ausman LM, Carrasco W, Gaultieri LJ, Jenner JL, Ordovas JM, Nicolosi RJ, Goldin BR, Schaefer EJ: Rice bran oil consumption and plasma lipid levels in moderately hypercholesterolemic humans. Atheroscler Thromb 14: 549–556, 1994.[Abstract/Free Full Text]
  32. Allain CC, Poon LS, Chan CSG, Richmond W, Fu PC: Enzymatic determination of total serum cholesterol. Clin Chem 32: 611–614, 1986.[Abstract/Free Full Text]
  33. Bucolo G, David H: Quantitative determination of serum triglycerides by the use of enzymes. Clin Chem 36: 476–482, 1973.
  34. Warnick GR, Benderson J, Albers JJ: Dextran sulfate-Mg2+ precipitation procedure for quantitation of high density lipoprotein cholesterol. Clin Chem 28: 1379–1388, 1982.[Free Full Text]
  35. Rogers EJ, Rice SM, Nicolosi RJ, Carpenter DR, McClelland CA, Romanczyk LJ Jr: Identification and quantitation of {gamma}-oryzanol components and simultaneous assessment of tocols in rice bran oil. J Amer Oil Chem Soc 70: 301–307, 1993.
  36. SAS Institute Inc.: "SAS-STAT Guide for Personal Computer, Version 6." Cary, NC: SAS Institute Incorporated, pp 398, 1985.
  37. Nicolosi RJ, Stucchi AF, Kowala MC, Hennessy LK, Hegsted DM, Schaefer EJ: Effect of dietary fat saturation and cholesterol on LDL composition and metabolism. Atheroscler Throm 10: 119–128, 1990.
  38. Kuo PC, Rudd MA, Nicolosi RJ, Loscalzo J: Effect of dietary fat saturation and cholesterol on low density lipoprotein degradation by mononuclear cells of cebus monkeys. Atheroscler Throm 9: 919–927, 1989.
  39. Spady DK, Dietschy JM: Interaction of dietary cholesterol and triglycerides in the regulation of hepatic low density lipoprotein transport in the hamster. J Clin Invest 81: 300–309, 1988.
  40. Spady DK, Dietschy JM: Dietary saturated fat triacylglycerols suppress hepatic low density lipoprotein receptors in hamsters. Proc Natl Acad Sci USA 82: 4526–4530, 1985.[Abstract/Free Full Text]
  41. Rong N, Ausman LM, Nicolosi RJ: Oryzanol decreases cholesterol absorption and aortic fatty streaks in hamsters. Lipid 32: 303–309, 1997.



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