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Foster Biomedical Research Laboratory, Brandeis University, Waltham, MA 02254
2To whom correspondence should be addressed. E-mail: kchayes{at}brandeis.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • structured triglyceride • stearic acid • energy value • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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), consumer demand in recent years has generated reduced-energy fats that mimic the taste and melting characteristics of traditional fat containing 38 kJ/g (9 kcal/g) (2
). Two types of low-energy fat replacements are available: mimetics based on carbohydrates and proteins, and lipid-based substitutes based on triglyceride (TG)3
structure modification. Mimetics successfully lower energy to 17 kJ/g (4 kcal/g) but, because they are not true fats, they typically are neither as functional nor as palatable as desired (2
). Reduced-energy, lipid-based fat substitutes are more desirable when their melting capacity, taste and mouth-feel closely resemble the fats they replace.
A group of reduced-energy structured TG (STG) [short and long acyltriglyceride molecules (SALATRIM)] is currently incorporated into foods. These STGs are thought to provide a mean of 21 kJ/g (5 kcal/g) digestible energy compared with 38 kJ/g (9 kcal/g) in natural fats (2
). Reduced energy is achieved by interesterification, where one or two of the long-chain fatty acids [LCFA; e.g., 16 or 18 carbon fatty acids (FAs)] in conventional fats and oils are replaced with lower-energy, SCOA, acetic (2:0), propionic (3:0) and butyric (4:0), to form dilongs (two LCFA per TG) and monolongs (one LCFA per TG). The major LCFA in SALATRIM is 18:0, which gives solidifying properties and plasticity to the resulting fats and enables the monoglyceride (MG) and diglycerides (DG) formed during digestion of SALATRIM to remain relatively solid at body temperature. Fecal excretion is enhanced, which reduces absorbed energy. The SCOA may further reduce the availability of stearic acid (3
).
Stearic acid is the preferred LCFA in reduced-energy fats because, as clearly demonstrated in rats (4
), it is poorly absorbed and does not adversely affect the plasma lipid profile in most species, including humans (5
). Mattson (6
) first found that FA absorption from TG containing 18:0 and oleic acid (18:1) depended on the amount and position of 18:0 on glycerol. He compared either simple mixes, or randomly interesterified TG mixtures, of safflower oil [largely trilinolein (LLL)] with fully hydrogenated linseed oil (tristearin, SSS). Addition of dietary Ca2+ and Mg2+ caused soaps to form with free FAs in the gut, thereby reducing FA absorption. Brink et al. (7
) demonstrated in rats that a specific TG molecular species, OSS (oleic, stearic, stearic), results in more absorbed stearic acid than SOS, especially at high calcium intake. Review of the literature supports this observation (3
,8
).
Similar to Mattson (6
), several studies on 18:0 absorption compared tristearin with other monoacyl TGs containing a single FA moiety (tripalmitin, triolein, etc.) to estimate absorbability of 18:0 relative to other FAs. For example, Clifford et al. (9
) reported that rats fed a tristearin-rich diet ate more, yet gained less weight, than rats fed corn oil. The digestibility of tristearin was only 20% that of corn oil, and excretion of fecal lipids was several times normal, i.e., 1000 mg/d versus 100–225 mg/d for trimyristin, LLL, or partially hydrogenated soybean oil.
The energy values of selected SALATRIM were studied previously in rats by the slope-ratio assay (10
). Restricted food intake limited basal growth 50%, and test fats were added in increments to assess the linearity of energy available for growth. The extreme restriction in food intake and changes in the quality and structure of test fats, coupled with the changing percentage of fat energy as increments of the test fat are added, raise several nutritional considerations, especially if the test fat is potentially atypical (such as STG). Thus, we designed a fat bioassay that allowed 
70–80% normal weight gain with dual purposes in mind. One was to use this novel bioassay to reassess SALATRIM energy values, including some not previously examined. The second was to provide further information about 18:0 availability when presented as various mono-, di- or triglycerides in a rat model for comparison with human studies.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Two experiments were conducted using a novel fat bioassay in which total fat intake was constant and balanced. Expt. 1 compared the energy value of a control American Heart Association (AHA) fat blend to cocoa butter, a natural fat rich in 18:0 and 16:0, and two STG rich in 18:0. The control AHA blend contained an equal amount of saturated, monounsaturated and polyunsaturated FAs, and the three test fats were mixed into the AHA blend at a ratio of 3:1. Blending the AHA fat blend with each test fat with gentle heat and stirring ensured enough normal fat for essential biological activities, including the metabolism of the test fat itself. All diets provided 33% energy as fat (Table 1
). Weanling rats fed the control AHA diet were food restricted to allow 80% of normal maximum growth in rats consuming food ad libitum (AHA 80%), and the three other groups were pair fed (on a group basis) to the AHA 80% group.
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). Unlike the study of Finley et al. (10
) and a classic slope-ratio assay for fat per se (11
), where several nutritional relationships are varied simultaneously, the fat:protein plus carbohydrate, fat:vitamin and fat:mineral ratios were kept constant in the present study, so that fat quality was the only variable.
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Sprague-Dawley male rats were obtained from Charles River Breeding Laboratories (Wilmington, MA) as weanlings (21 d and 60 ± 2 g) and were immediately fed the experimental diets. Each was individually housed and fed a weighed amount of food daily. The amount fed to all groups (except AHA-60%) was set as that necessary to keep body weight of rats fed the AHA-80% diet (80% controls) to a preset curve that described an 80% growth rate (5.2 g/d for 4 wk). Because maximal body weight for 49-d-old males in this strain is 260 g (Fig. 1)
, the final 80% target weight for the AHA-80% group (Expt. 1) was 208 g, whereas the target weight for the AHA-60% group (Expt. 2) was 156 g. All rats had free access to water. Body weights were recorded every 2–3 d. Feces were collected beneath wire-bottom cages for 3 d at the end of the study.
Test materials.
All samples of SALATRIM TGs (Benefat 1, 3, M and X2); Myverol, a commercial MG (monostearin) from Eastman Chemicals; and Glyceride 1237, a synthetic DG (distearin) prepared at Danisco (Brabrand, Denmark) were provided by Danisco-Cultor (Ardsley, NY).
Diets.
The actual diet formulas (Table 1)
and the dietary FA composition and TG structure (Table 2
) are described. The purified diets were prepared as a starch gel that contained 40% water as fed (based on several analyses of diets at the time of feeding). This water was accounted for when generating the mean dry weight of food fed each day in the two studies. With the exception of diet 5 (Expt. 2), which was designed to restrict growth to 60% normal, all other diets were allotted at 19 g/d (wet weight) on average throughout the 28-d experiment, because this amount generated 80% growth (Fig. 2
) in control rats (diet 1). Each diet provided the same amount of vitamins, minerals, fiber, protein, fat and carbohydrates, with the only difference being the test fat that was mixed with the AHA fat blend.
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On d 28, rats were food deprived for 16 h before obtaining blood by cardiac puncture while they were under O2/CO2 anesthesia. After exsanguination, the liver, cecum and right perirenal adipose tissue were dissected and weighed. Total plasma cholesterol and TGs were determined by enzymatic assays (Sigma Diagnosis kit, procedure no. 352 for cholesterol and no. 336 for TGs; Sigma-Aldrich, St. Louis, MO). During the last week of feeding, feces were collected for 3 d and fecal fat (12
) and FA profiles (13
) were determined after drying, pulverization and three extractions by the Folch procedure (14
). All protocols and procedures were approved by the Brandeis University Animal Care and Use Committee.
Statistics.
Statistical analysis was performed on a Macintosh Power PC (Apple Computer, Cupertino, CA) using StatView 5.0.1 (SAS Institute, Cary, NC). Data were analyzed by one-way analysis of variance and Sheffe’s F-test. Results were expressed as mean ± SD and differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). This translated into a 5.21-g weight gain per day in rats with an intake of 199 kJ/d provided by 19 g (wet weight) of control diet. In Expt. 2 (Table 3)
, growth for rats fed the control 60% AHA fat blend diet also was close to the desired 60% normal growth (154 g at 4 wk). This was accomplished by feeding 14 g/d food (wet weight) to provide 144 kJ, which resulted in 3.28 g/d weight gain. Each of the test fats from Expts. 1 and 2, including cocoa butter, was presented in 19 g (11.6 g/d dry food) of food, and each generated a lower daily weight gain than the AHA 80% control diet (Table 3
and Fig. 2
).
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also compares daily body weight gain (x-axis) with the total daily energy intake (y-axis). A standard curve was generated by the two fixed points of known energy intakes (60% AHA and 80% AHA, each providing 144 or 199 total kJ/(g/d), respectively, based on 38 kJ/g fat consumed). Using this slope allowed calculation of the total daily energy supplied by each test diet based on the observed weight gain. Calculating energy value.
All rats were weighed every 2–3 d, and the mean weight gain per day for the entire period was calculated and compared with the amount of food consumed. Knowing the exact composition of the diet (amount of protein plus carbohydrate and fat), it was possible to calculate an energy value for the test fat, "X, " by using weight gain per day to estimate the daily total energy intake (EI) from the standard curve (Fig. 2)
. The equation was then solved for X (STG energy value) as follows: EI (kJ/d) = (0.685 x 16.72)* + (0.0375 x 37.62)** + (0.1125 x "X")*** x (g/d food intake); * indicates the amount of protein + carbohydrate per gram of diet x energy in kJ, ** indicates the amount of AHA fat blend per gram of diet x energy in kJ, and *** indicates the amount of STG per gram of diet x energy in "X" kJ.
Solving for X, we used the following equation: X (energy value of test fat in Kj/g) = (EI - 12.86 x g/d food)/(0.1125 x g/d food).
Based on dry weight food intake of 11.61 g/d in Expt. 1, the equation was X = (EI - 149.3)/1.3.
For Expt. 2, where dry weight food intake was 11.30 g/d, the equation was X = (EI - 145.3)/1.27.
The actual metabolizable energy value for each glyceride is presented in Table 2
and ranged from 30 kJ/g (7.1 kcal/g) for cocoa butter to 12 kJ/g (2.9 kcal/g) for the DG, distearin.
Organ weights (relative or absolute) did not differ among groups, except for adipose reserves in Expt. 1 (diet 3) and the liver weight of the 60% AHA control group (diet 5) in Expt. 2 (Table 3
, absolute values not shown). In fact, the relative adipose weight generally followed the pattern of reduced weight gain among all rats. Plasma cholesterol and TG concentrations were not affected by diets, except plasma cholesterol was higher in the AHA 60% restricted controls than in most other groups in Expt. 2.
The level of 18:0 (g/100 g) in test fats and in dried feces (g/d) were each inversely related to the energy value of fat (r = -0.90; P < 0.001; and r = -0.92; P < 0.001, respectively), but total fecal fat was unrelated to the energy value of fat. With the exception of glyceride 1237 and Myverol, there were no relationships between the fat energy and fecal 18:0 output. Fecal excretion of 16:0 was highest in rats fed the 60% and 80% AHA blends (diet 2, Table 4
), whereas daily fecal excretion of 16:0 was not affected in rats fed SALATRIM fats (diets 3, 4 and 6–9).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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This energy evaluation confirms that STG in the SALATRIM family have reduced available energy, with a mean value of 22 kJ/g (5.2 kcal/g) for the four SALATRIM (Benefat 1, 3, M and X2) tested. Restriction to 80% of maximal growth still allowed these rats to grow steadily at the lower limits of normal growth for this rat strain (Fig. 1)
. In fact, liver weight was normal, with only adipose reserves being limited by these four diets. The reduced liver weight in rats fed the 60% AHA control (diet 5) suggests that this group represented a less desirable control, although it was an important anchor for the standard curve. Our 4-wk test period also reduced the variation contributed by day-to-day inconsistencies in food intake that might affect a shorter study.
The model used a novel design to minimize stress by ensuring a balanced dietary fat and total energy sufficient for low but normal growth. As such, it deviates from the classical slope-ratio assay, which adds increments of a specific fat to a severely restricted basal diet while assessing carcass (and feces) for energy retained as a function of the increasing fat intake (10
,11
). A shortfall would occur with the classical assay if the fat or energy restriction were too severe or if the fat (e.g., a STG) had attributes other than as an energy source. For example, feeding tristearin as the only fat could limit EFA and modify lipid metabolism, confounding an energy effect. To guard against this possibility, our model kept fat constant at 30% of energy and allowed an overall growth rate of 80% normal. This approach minimized the stress of energy restriction whereas one fourth of the fat was incorporated as an AHA standard blend to ensure FA balance and EFA sufficiency. The rationale and concern for aberrant lipid metabolism under such conditions is based in part on two observations. The first is that the effects of saturated FAs on lipoprotein metabolism are modulated by the concurrent linoleic acid intake (15
,16
). The second is that very low fat (energy) per se can impair fat use (3
).
Energy values from the bioassay.
Our bioassay estimated the energy from each test fat relative to the 38 kJ/g (9 kcal/g) assigned to the AHA fat blend. As predicted, energy was inversely related to the amount of 18:0 in the glyceride. Based on growth, the best absorbed fats were Benefat 3, Benefat 1, and the non-SALATRIM MG, Myverol, all of which are primarily 18:0-monolongs. Surprisingly, Myverol had a higher energy value than its high proportion of 18:0 might predict, indicating that randomized monolong-18:0 was relatively available when dispersed in normal fat. Adding another 18:0 to form dilong-18:0 substantially depressed availability, as demonstrated by Benefat X2, Benefat M, and glyceride 1237, which contained mostly dilong-18:0 structures and produced lower weight gains. By contrast, forming a TG by adding two butyric acids to an 18:0 MG (Benefat 3) increased available energy 14% compared with Myverol, whereas adding a lesser amount of primarily acetate (Benefat 1) decreased the energy available by 7%.
Cocoa butter was chosen as a control representing a natural fat containing stearic acid, typically as POS and SOS (17
). The growth data show that the natural dilong SOS, with 18:0 representing only 34 g/100g total FAs, provided more energy than other randomly structured dilong-18:0 TG containing SCOA, in which the proportion of 18:0 was much greater. Randomization of 18:0 from its natural SOS configuration enhances availability (6
,7
), indicating that the location of 18:0 on the TG molecule affects its absorption. For example, Brink et al. (7
) found that SOS was absorbed less and excreted more than SSO, particularly when calcium intake enhanced soap formation. Our energy value for cocoa butter (30 kJ/g, 7.1 kcal/g) was 79% that of the AHA blend and slightly greater than the 72% reported for rats by Finley et al. (10
). The difference may reflect our longer trial (4 wk versus 2 wk), less severe energy restriction (20 versus <50%) and the percentage of test fat to total fat (75 versus 50–81%). Nonetheless, both assays are based on the assumption that growth in rats during this period is both linear and directly related to the available energy.
Fecal fat versus growth for estimating fat energy.
Compared with our use of fat digestion and absorption to affect growth in rats, a human study used fecal excretion as its index of 18:0 absorption (18
). In that study, 30 g of cocoa butter (at 30% of the total dietary fat compared with our 75%) appeared to be as digestible as corn oil (similar fecal fat output) when added to a normal diet of adults. By contrast, when reduced-energy SALATRIM were fed to rats, an exceptionally large quantity of total fat and 18:0 was recovered in the feces (10
), suggesting atypical fat excretion. It is well documented that 18:0 fed as tristearin is poorly absorbed (6
,9
), which is also true of SALATRIM formulations containing tristearin (2
,19
). Pai and Yeh (20
) reported that 18:0 was poorly incorporated into phospholipid molecules (<10% relative to 14:0, 16:0 and 18:1) with a high rate of incorporation into MGs and DGs in hepatocytes. This suggests that more 18:0 remains free in the cell and is poorly metabolized compared with other FAs, providing a basis for its reduced absorbability when mucosal cells slough. However, in our study neither fecal fat nor fecal 18:0 predicted the energy available in the test fat, with the exception of glyceride 1237 (with its high 18:0-dilong content). For example, the 18:0-MG, Myverol, increased fat and 18:0 excretion but yielded a moderate energy value, and diet 6 (Benefat X2 with 82% dilong-18:0) yielded a low energy value but was associated with average excretion of fecal 18:0 and total fat.
Klemann et al. (19
) also noted the inconsistent absorbability of 18:0 and thought it reflected the short:long (S:L) molar ratio (with 4:0 acid as the SCOA), i.e., the greater the ratio, the more 18:0 absorbed. This positive association between energy value and SCOA in SALATRIM was also noted by Finley et al. (10
) and concurs with our data on S:L molar ratios that included STG with 2:0 and 3:0, in addition to 4:0 (Table 2)
. For example, Benefat X2 had a low energy value and S:L ratio of only 0.58 while Benefat 3 had a high energy value and a S:L ratio of 1.78, with Benefat 1 and Benefat M intermediate. In contrast, the S:L relationship may simply reflect the dilong content of test fats, because a high dilong configuration would have a low S:L molar ratio. It appears that 2:0 may reduce the energy available from 18:0 more than 4:0, because Benefat 3 with a high 4:0 content provided appreciably more energy than Benefat 1. This concurs with the findings of Finley et al. (10
).
Total fat and 18:0 availability.
Our data, coupled with literature data, imply that the availability of 18:0 from mono-, di- or triglyceride molecules depends on a fat mass effect that may reflect 18:2 intake available for lipid metabolism. Apgar et al. (12
) observed that the digestibility of cocoa butter in rats was lower than that of corn oil, but digestibility increased from 59 to 72% as the total percentage of fat in the diet increased from 5 to 20%. Thus, the studies of Finley et al. (10
) and Klemann et al. (19
) are noteworthy because the fat content of their natural-ingredient diet was <5% before the addition of test fat, and fecal stearate was 15- to 20-fold greater than our results and the literature norm. The energy estimates for two of their SALATRIM fats (23CA and 4CA) were less (4 kJ/g) than values we obtained for similar fats (Benefat 1 and Benefat 3). Thus, the low fat content (and 18:2 availability) of their basal diet, coupled with their 50% energy restriction, may have limited fat digestion and increased 18:0 excretion in the feces.
Similarly, it can be argued that the higher percentage 18:0 in a test fat and the lower proportion of natural fat in the diet, the less likely that 18:0-TG will be digested fully. This may explain why human studies, by their very nature, using diets with more total fat intake and proportionately less test fat (typically less than half the total fat), generally report higher availability of 18:0 than rat studies. In rat studies, 18:0 usually represents a larger portion of the total FAs, often in relatively low-fat diets (10–20% of energy) compared with 30–40% of energy as fat in human studies. Thus, impaired digestion and malabsorption of a STG would be less likely to occur in most human studies (5
,18
), where fat and 18:2 intake are relatively high. In contrast, a human study demonstrated only 89% absorbability for cocoa butter when it was the sole fat in a high-fat diet, which would indicate limited 18:2 consumption (21
).
Humans versus rats.
In addition to differences in relative fat intakes, the apparent discrepancy between 18:0 availability from fats in humans (typically >90%) and rats (<75%) probably relates to differences in diet design and assays used to assess 18:0 absorption in the two species. A rat growth assay is more direct and compelling as a true estimate of available energy from 18:0-rich fats. It offers better control over the absolute amount and quality of test fat and uses the linear growth period to measure energy available from a specific fat. In contrast, having complete control over diet composition runs the risk of design flaws, e.g., when insufficient total fat or polyunsaturated FA may inadvertently bias the outcome. By contrast, the typical assay for estimating unabsorbed 18:0 energy in adult humans incorporates a relatively limited amount of test fat and depends on fecal collection as well as isolation and quantitation of 18:0 in feces.
As evidenced by the current study, fecal analysis represents a rather obtuse, hard to quantify endpoint for determining available dietary stearate, a process that is further complicated in humans, where the percentage of daily energy from fat tends to be greater. In fact, review of the literature suggests that attempts to determine 18:0 available from dietary fat in humans is fraught with problems. These include such factors as uncontrolled consumption of too few or too many other fats (FAs) relative to the test fat, incomplete fecal collection and extraction, variable intake of minerals such as calcium and the mixing or exchange of FAs derived from the intestinal mucosa. These considerations compromise the analysis as well as estimations of FA absorption and energy available. Thus, ordinarily the adult human would seem to represent a poor system for estimating actual 18:0 absorbability from test fats, whereas rats would be more accurate only when the total dietary fat profile has been carefully considered.
Despite the above caveats, a carefully designed and executed human study found that the coefficient of absorption for 18:0 in SALATRIM 23CA was 68% in humans (22
), which is similar to the 64–72% reported for rats by Hayes et al. (23
). Finally, experiments conducted by Filer et al. (24
) showed that randomization of FAs in lard incorporated in human infant formula (low 18:2) resulted in18:0 absorbability declining from 88 to only 40%. Because fat intake and fecal collection were well documented, the striking decline in 18:0 absorption must reflect altered TG structure, possibly confounded by the dual limitations imposed by the low 18:2 content of lard and an immature human digestive tract.
Cocoa butter and plasma lipids.
Kritchevsky (25
) reviewed the special qualities of cocoa butter relative to its lack of cholesterol-raising activity and lower incidence of atherosclerosis in animal models. Compared with other saturated FAs containing 16:0 and 20:0, he attributed the low cholesterol raising potential of cocoa butter to the poor absorbability of 18:0. Schneider et al. (26
) demonstrated that endogenous cholesterol excretion in hamsters was almost twice as great when 18:0 was compared with 16:0, 18:1 or 18:2, all as monoacylglycerides. The inference was that poorly digested tristearin may disturb micelle formation in the gut, resulting in an altered bile acid profile and reduced cholesterol absorption, which, in turn, lowers plasma cholesterol.
Plasma lipids were not affected by 18:0-rich SALATRIM in our study, which is similar to results in humans (27
,28
). Others have reported various effects for other 18:0-rich fats. Imaizumi et al. (29
), like Schneider et al. (26
), found that cholesterol absorption decreased in cholesterol-fed rats consuming high dietary 18:0 compared with 16:0. However, this decrease was countered by increased whole-body cholesterol production (26
). Dougherty et al. (5
) agreed that 18:0 from sheanut oil (SOS) does not increase plasma total cholesterol in humans, and also found that 18:0 absorption decreased 8% during high stearate consumption (at 7.3% of energy) versus low stearate consumption. Although no change occurred in plasma cholesterol with the test fats in the present study, Myverol (diet 7, Table 4
) significantly increased fecal cholesterol output compared with other groups, which presumably reflects its high monostearin content.
In summary, a novel fat bioassay was implemented to define energy available from mono-, di- and triglycerides with one or two randomly positioned 18:0 molecules for comparison with natural cocoa butter. The results confirm that 18:0 is less well absorbed than other FAs, that increasing the 18:0 content of a glyceride decreases its available energy and that growth was a better predictor than fecal 18:0 excretion. Although technically feasible, such human studies would appear more difficult to execute and less likely to be as accurate as a properly designed rat experiment.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: AHA, American Heart Association; DG, diglyceride; FA, fatty acid; LCFA, long-chain FA; LLL, trilinolein; MG, monoglyceride; O, oleic; S, stearic; SALATRIM, short and long acyltriglyceride molecule; SCOA, short-chain organic acid; S:L, short:long; STG, structured triglyceride; TG, triglyceride.
Manuscript received 26 December 2001. Initial review completed 5 February 2002. Revision accepted 5 August 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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