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© 2006 American Society for Nutrition J. Nutr. 136:1209-1214, May 2006

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

The Conversion Efficiency of trans-11 and trans-12 18:1 by {Delta}9-Desaturation Differs in Rats1,2

Jana Kraft*, Laura Hanske*, Peter Möckel*, Sindy Zimmermann*, Albert Härtl{dagger}, John K. G. Kramer** and Gerhard Jahreis*,3

* University of Jena, Institute of Nutrition, 07743 Jena, Germany; {dagger} Leibniz Institute for Natural Product Research and Infection Biology-Hans-Knöll-Institute, 07745 Jena, Germany; and ** Food Research Program, Agriculture and Agri-Food Canada, Guelph, ON, Canada

3 To whom correspondence should be addressed. E-mail: gerhard.jahreis{at}uni-jena.de.


   ABSTRACT
TOP
 ABSTRACT
MATERIAL AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
The present study evaluated and compared the efficiency of the conversion of t11 18:1 and t12 18:1 to their corresponding dienoic acids (c9,tn 18:2) and assessed whether differences due to gender existed in several tissues of rats. Three groups of 4-wk-old male and female rats were fed for 3 wk a diet supplemented with 0, 0.5, or 1% of a trans-octadecenoic acid isomer mixture (tOIM) containing t11 18:1 and t12 18:1 in equal proportion. t11 18:1 and t12 18:1 were incorporated in a tissue-specific manner, and the accrual was significant with increased dietary intake of these trans fatty acid (tFA) isomers. The t12 18:1 isomer was more readily incorporated into the rat tissues than the t11 18:1 isomer. From t11 and t12 18:1, the respective desaturase products, c9,t11 18:2 and c9,t12 18:2, were formed. The calculated conversion rates varied greatly among the tissues of the rats but they were consistently lower for t12 18:1 than for t11 18:1, suggesting that t12 18:1 is a poorer substrate than t11 18:1 for {Delta}9-desaturase. For both fatty acids investigated, the calculated conversion rates in decreasing order of conversion efficiency were: testes = kidneys > adipose tissue > ovaries > muscle > liver > heart. Overall, there were distinct differences in the conversion of t11 18:1 and t12 18:1, indicating that these 2 fatty acids are metabolized differently despite their structural similarities. Such metabolic differences in tFA accumulation and metabolism may have potential implication in assessing the safety of these tFA isomers because there is a positive correlation between the intake of tFA and the incidence of various diseases.

KEY WORDS: • trans fatty acids • t11 18:1 • t12 18:1 • {Delta}9-desaturation • rats • tissue • gender

In recent years, trans fatty acids (tFA)4 have received renewed attention because of the strong relation between their dietary intake and adverse implications for cardiovascular disease (1) and immune functions (2,3). tFA originate from the following: 1) biohydrogenation of unsaturated fatty acids by microorganisms of ruminants; 2) industrial partial hydrogenation and deodorization of vegetable and marine oils; and 3) heating fats at high temperature during food preparation. In human diets, the most common tFA belong to the group of octadecenoic acids (18:1) consisting of a large number of positional isomers [t4 to t16 18:1; (4,5)]. Industrial and ruminant fats contain the same trans 18:1 isomers; however, the relative distribution differs greatly between the 2 sources. t11 18:1 is the major isomer of ruminant fats (40–70% of total trans 18:1) together with t13/14, t9, t10 and t12 18:1 (6–8). In contrast, the trans 18:1 isomeric profile of industrial fats appears to be almost Gaussian-like with t6-t8, t9, t10, t11, and t12 18:1 as predominant isomers (4,9–12). Estimates of daily tFA intakes range from ~1.3% (EU) to 2.6% (USA) of total energy (13,14). However, no published data regarding the daily intake of single tFA isomers are available at present. Evidence is accumulating that it not simply the total intake of tFA that is of crucial importance in the development of increased risk factors of human cardiovascular diseases, but rather, the intake of specific tFA isomers. The position of the trans-double bond may exert distinct physiologic and metabolic effects. Because tFA are commonly present in the human diet, despite current efforts to decrease their content by reformulation of food items, the fate of tFA in the diet is becoming an important health question. After digestion and absorption, tFA can be incorporated into tissues and/or metabolized by desaturation, elongation, or oxidative degradation processes. Theoretically, trans 18:1 may undergo desaturation to their corresponding cis/trans dienoic acid, although the cis 18:1 isomers are the preferred substrates for desaturases (15). This reaction is catalyzed by the microsomal enzyme {Delta}9-desaturase [EC 1.14.99.5; also commonly known as stearoyl-CoA desaturase (SCD)] by insertion of a cis-double bond at the {Delta}9 position of the fatty-acyl chain. In vitro studies suggest that some trans 18:1 isomers are good substrates for {Delta}9-desaturase, except t8, t9, and t10 18:1 (16,17). Although data on the endogenous conversion of t11 18:1 to c9,t11 18:2 in tissues have been published, very limited data are available concerning the endogenous conversion of t12 18:1 to c9,t12 18:2 in tissues. The purpose of this investigation was to evaluate and compare the contribution of dietary t11 18:1 and t12 18:1 to their desaturase products, c9,t11 18:2 and c9,t12 18:2, respectively, using rats as a model in an attempt to determine tissue and gender-specific differences.


   MATERIAL AND METHODS
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 ABSTRACT
 MATERIAL AND METHODS
RESULTS
 DISCUSSION
 LITERATURE CITED
 
    Animals, diets, and study design. Permission for the experiment was given by the Thueringer Office for Food Safety and Consumer Protection, Department of Sanitary Consumer Protection and Veterinary Care according to article 8.I of the Animal Welfare Act. The rats were obtained from the Institute of Pharmacology and Toxicology of the University of Hanover at 32 d of age. Hanwist rats (n = 24; 12 male, 12 female) were randomly assigned within gender to 3 groups of 8 (4 male, 4 female) and fed different doses of a trans-octadecenoic acid isomer mixture (tOIM; 0% control, 0.5% and 1.0% by weight). The preparation (Natural ASA) was comprised of equal amounts of t11 and t12 18:1 that totalled 64% of all component fatty acids. The fatty acid composition of this preparation was provided by the supplier and verified in our laboratory. Soybean oil was added to the control and 0.5% tOIM diets to make the diets isoenergetic. Rats were fed a purified rodent diet based on the recommendations of the ASN described elsewhere (18,19). The supplemented diets contained 1.8 g/kg diet (0.5% tOIM) and 3.6 g/kg diet (1% tOIM) t11 18:1 and t12 18:1 each, respectively. The freshly prepared diets were proportioned in appropriate amounts and stored at –20°C until needed. Throughout the study (21 d) rats were given free access to both feed and water; they were maintained on a 12-h light:dark cycle at ambient room temperature of 24°C and 60% humidity. After delivery, the rats were kept in individual plastic cages and acclimated for 9 d to the diet and facility. On d 10, rats were transferred to metabolism cages equipped with wire mesh bottoms and collection trays. Urine and feces were quantitatively collected for a period of 5 d at the end of the experiment. Excreta were pooled, homogenized, and stored frozen at –80°C until analyzed. Body weight and feed consumption (offered – refused) were monitored daily. Feed efficiency was calculated from food consumption and weight gain data during the 3-wk experimental period. At the termination of the study, rats were anesthetized with CO2 and exsanguinated. Tissues (adipose tissue, liver, heart, kidneys, muscle, and gonads) were excised quickly, weighed, and stored at –80°C until analyzed.

    Fatty acid analysis. Tissue and feces samples were lyophilized and pulverized in a laboratory grinder (Janke & Kunkel). Total lipids were extracted according to the method of Folch et al. (20) using a mixture of methanol:chloroform:water (1:2:1, by vol). A known amount of tricosanoate (triacylglycerol 23:0), as an internal standard for quantification, was added to each isolated lipid extract before the methylation stage. The lipids were transesterified with anhydrous 1,1,3,3-tetramethylguanidine in methanol (1:4, by vol) for 5 min at 100°C as reported by Schuchardt and Lopez (21). The resultant FAME were purified by TLC on silica gel plates (Merck) using a mixture of hexane:diethyl ether:acetic acid (80:10:1, by vol). Samples were then analyzed by 2 GC procedures and silver-ion HPLC (Ag+-HPLC) as described previously (8). The use of 2 different GC procedures was required to obtain a complete resolution of all fatty acids including cis- and trans-18:1 isomers (8). Ag+-HPLC separation was mandatory for resolution of conjugated 18:2 isomers.

    Estimation of the t11 and t12 18:1 conversion rates. To evaluate the conversion of t11 18:1 and t12 18:1 to c9,t11 18:2 and c9,t12 18:2, respectively, the net changes of those fatty acids were calculated. The net change represents the difference between the tissue fatty acid concentrations in rats fed tOIM and those in rats fed the control diet. The slope of the linear regression of the net change of {Delta}9-desaturase product vs. the sum of the net change of {Delta}9-desaturase substrate and the net change of {Delta}9-desaturase product represents the average of the conversion rate. The conversion rate of t11 and t12 18:1 to c9,t11 and c9,t12 18:2, respectively, in tissues was calculated according to the formula of Palmquist and Santora (22) as follows:

Formula

    Statistical analyses. The results are presented as means ± SD. Data were analyzed using the statistical software package SPSS for Windows Version 11.5. After testing for homogeneity of variance and normality, 2-way ANOVA was used to determine the effects of diet and gender and their interaction for the measured fatty acid levels and separately for each tissue. When there was no significant effect of gender, the means for male and female rats were collapsed and 1-way ANOVA was used for comparison among the different diet groups. When ANOVA was significant, post hoc testing of differences between groups was performed using Scheffé‘s test. Student’s t test was used separately to compare differences in the levels of the fatty acid isomers examined (t11 18:1 and t12 18:1; c9,t11 18:2 and c9,t12 18:2) in each tissue. In the case of the conversion rate, group comparisons among the diet groups (0.5 and 1% tOIM) and gender (male and female) were also tested by Student's t test. Differences were considered significant at P < 0.05.


   RESULTS
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 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
DISCUSSION
 LITERATURE CITED
 
    Food intake and body weight. Food intake and food efficiency did not differ among the diet groups, but there were gender differences; male rats consumed significantly more food than female rats (Table 1). Body weights and daily weight gains were not affected by treatments but they were significantly lower in female rats than in male rats.


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  		TABLE 1 Feed intake, body weight, and weight gain of male and female rats fed control or tOIM-enriched diets for 3 wk1

 
    Fatty acid composition of tissue lipids. {Delta}9-Desaturase catalyzes the conversion of t11 18:1 and t12 18:1 (substrate) to c9,t11 18:2 and c9,t12 18:2 (product), respectively. Rats that consumed tOIM had greater proportions of t11 18:1 in all tissues compared with controls (P < 0.05). Increasing the amount of tOIM from 0.5 to 1% of the diet significantly increased t11 18:1 in all tissues except for heart and liver. The level of t11 18:1 generally increased from <0.5% when the control diet was fed to a maximum of 12% of total lipids in adipose tissue (Fig. 1 A); the lowest level of t11 18:1 was in the kidneys. The accumulation of t11 18:1 did not differ between genders except for those levels in gonads. The ovaries accumulated the highest level of t11 18:1, nearly twice that found in the testes (0.5% tOIM: 23.88 µmol/g fat; 1% tOIM: 43.58 µmol/g fat for males vs. 0.5% tOIM: 41.62 µmol/g fat, 1% tOIM: 88.67 µmol/g fat for females).


Figure 1
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  		FIGURE 1  Concentration of t11 18:1 (panel A) and t12 18:1 (panel B) in different tissues of rats fed control or tOIM-enriched diets for 3 wk. Values are means ± SD. Data for male and female rats were pooled (n = 8) because there were no gender differences, except for the gonads (n = 4). There was a significant diet effect (P < 0.05) for all tissues. Within each diet group, values not sharing the same letter differ, P < 0.05. Abbreviation: AT, Adipose tissue.

 
The t12 18:1 isomer was found only at trace levels in the control group (Fig. 1 B). Even though t11 18:1 and t12 18:1 were present in the same relative proportions in the tOIM-enriched diets, the accumulation of t12 18:1 was higher than that of t11 18:1 in each tissue and notably higher in the liver. Increasing the dietary supply of tOIM significantly increased the t12 18:1 concentration in all tissues except for heart and liver, similar to the results for t11 18:1. The highest accumulation of t12 18:1 occurred in the liver and the lowest levels were found in muscle and kidneys. There were no gender differences, with the exception of a greater accumulation of t12 18:1 in the ovaries in analogy to t11 18:1.

All of the basal diets were free of c9,t11 18:2 and c9,t12 18:2; therefore, these fatty acids in rat tissues were derived from the tFA supplement (tOIM). Increasing the dietary supply of t11 18:1 increased c9,t11 18:2 in a linear fashion in all of the tissues examined (Fig. 2 A). The highest levels of c9,t11 18:2 were found in the adipose tissue and gonads, and the lowest in liver and heart. There were no gender differences in the relative concentration of c9,t11 18:2 in any of the tissues examined, including the gonads. This was unexpected because t11 18:1, the precursor of c9,t11 18:2, was present at twice the relative concentration in the ovaries compared with the testis. The ratio of t11 18:1 to c9,t11 18:1 represents the conversion rate and will be discussed below.


Figure 2
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  		FIGURE 2  Concentration of c9,t11 18:2 (panel A) and c9,t12 18:2 (panel B) in different tissues of rats fed control or tOIM-enriched diets for 3 wk. Values are means ± SD. Data for male and female rats were pooled (n = 8) because there were no gender differences, except for the gonads (n = 4). There was a significant diet effect (P < 0.05) for all tissues. Within each diet group, values not sharing the same letter differ, P < 0.05. Abbreviation: AT, Adipose tissue.

 
The 9c,t12 18:2 isomer was not detected in the tissues of the control group. The progressive increase in the dietary supply of t12 18:1 increased the tissue c9,t12 18:2 concentrations (P < 0.05, Fig. 2 B). However, c9,t12 18:2 was generally present at only one-tenth the level of c9,t11 18:2, the {Delta}9-desaturase product of t11 18:1. The pattern of accumulation of c9,t11 18:2 in the different tissues was unlike that of c9,t12 18:2. Clearly, 9c,t12 18:2 accumulated at much greater levels in muscle and kidneys followed by liver, gonads, adipose tissue, and heart in decreasing abundance. There were no gender differences except for kidney and liver in which the levels were higher in males than in females.

    Fatty acid composition of fecal lipids. Feces of the control group contained t11 18:1 and t12 18:1, and the amount of t11 18:1 was 10 times higher than that of t12 18:1 (Table 2). Rats fed tOIM had greater amounts of t11 18:1 and t12 18:1 in fecal lipids than controls. However, the proportions of those fatty acids did not differ between rats fed 0.5 and 1% tOIM. c9,t11 18:2 was also present in feces of rats fed the control diet, but the level was significantly lower than that in the tOIM-supplemented groups. Furthermore, c9,t12 18:2 was not detected in fecal lipids of any treatment group. Overall, there were no significant gender-related differences in the fatty acid composition of fecal lipids.


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  		TABLE 2 Concentrations of the supplemented fatty acids (t11 18:1; t12 18:1) and their respective desaturase products (c9,t11 18:2; c9,t12 18:2) in feces of rats fed control or tOIM-enriched diets12

 
    Estimates of the relative conversion rates. Comparing the {Delta}9-desaturase substrates, t12 18:1 was substantially less desaturated than t11 18:1 (Table 3). Significant tissue differences were found in the conversion rates of both {Delta}9-desaturase substrates. The highest conversion rates of t11 18:1 and t12 18:1 were found in adipose tissue, kidneys, and ovaries and the lowest in heart. Elevating the dietary intake of tOIM increased the conversion rates as well. Moreover, the data indicate obvious gender differences in the conversion rate. Desaturation of t11 18:1 and t12 18:1 tended to be higher in the adipose tissue of female rats compared with male rats (P = 0.10), whereas they did not differ in muscle and were distinctly lower (P < 0.05) in all of the other tissues examined.


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  		TABLE 3 Estimates of the relative conversion rate of t11 18:1 to c9,t11 18:2 and t12 18:1 to c9,t12 18:2 in tissues of male and female rats fed 0.5 or 1% tOIM-enriched diets for 3 wk1

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
 DISCUSSION
LITERATURE CITED
 
This study was designed to compare the relative metabolism of 2 tFA in rats using a nonradioactive preparation because of the limited availability and prohibitive cost of labeled material. Furthermore, this study was limited to the determination of fatty acid incorporation and calculation of conversion rates that were estimated on the basis of the mean net change in end-product levels. The calculations do not account for many additional possibilities of fatty acid metabolism, such as elongation, desaturation, oxidative degradation, and tissue-specific turnover. Therefore, the estimated values do not reflect the real gross incorporation and conversion rate; rather, they represent the net sum of the remaining accumulated nonmetabolized fatty acids.

The results of this study showed that the dietary supplements t11 18:1 and t12 18:1 were incorporated at different degrees into the tissue lipids of the rats. The distribution of these 2 tFA in the tissue lipids differed markedly from the dietary composition, and varied in different tissues. Although adipose tissue and ovaries had the highest incorporation of t11 18:1, less was deposited in muscular tissues with a relatively high content of phospholipids, such as testes, kidney, heart, and skeletal muscle. The t11 18:1 isomer was preferentially deposited into triacylglycerols, in agreement with several other previous studies in rats (23–25). Generally, t12 18:1 was deposited to a greater extent than t11 18:1 in the rat tissues. The t12 18:1 isomer was preferentially incorporated into the liver followed by the heart, adipose tissue, and ovaries, whereas there appeared to be a discrimination of t12 18:1 into testicular lipids. The reason for the observed differences in tissue-specific accumulation of the 2 tFA is not clear. The incorporation of fatty acids into tissue lipids depends on the position and spatial configuration of the double bond (23). Furthermore, the characteristic pattern of the tissue-specific incorporation illustrates the selectivity of fatty acids in metabolism. Tissue fatty acid distribution is a dynamic system constantly receiving, metabolizing, oxidizing, and incorporating fatty acids. An increased accumulation of a fatty acid in the tissue could reflect selective uptake or slower metabolism, whereas a slight deposition might indicate a selective discrimination process or a more effective metabolization of this fatty acid (26). The high level of incorporation of both of these tFA into ovaries may be a result of reproduction processes characterized by an extensive fatty acid uptake by the ovaries for reproductive performance.

Early in vitro studies in liver microsomes revealed the conversion of several positional trans 18:1 isomers to c9,tn 18:2 fatty acids by {Delta}9-desaturase (16,17). A number of studies in different species such as rodents (25,27–29), pigs (30), chickens (31), cattle (32,33), and humans (34–36) established that t11 18:1 is utilized for endogenous synthesis of c9,t11 18:2. Investigations regarding the formation of c9,t12 18:2 from t12 18:1 are more limited. To date, only 1 study in dairy cows has verified this metabolic pathway (32). The results obtained in this study provide the evidence for the endogenous synthesis of c9,t11 18:1 and c9,t12 18:1 from t11 18:1 and t12 18:1, respectively. These data provide further evidence that t11 18:1 is effectively {Delta}9-desaturated (25,27,28). The enrichment of c9,t12 18:2 in all tissues investigated accompanied by increasing the amounts of t12 18:1 in the diets indicates the existence of a comparable pathway for the conversion of t12 18:1 to c9,t12 18:2. The present study shows clearly that t12 18:1 was desaturated at a much slower rate than t11 18:1. t12 18:1 was converted at a rate of ~2%, whereas the rate for t11 18:1 was ~20%. Similar results were found when lactating cows were supplied with a mixture of t11 18:1 and t12 18:1 by abomasal infusion (32). Changes in milk fat yield of t12 18:1 and c9,t12 18:2 accounted for 64% of the infused t12 18:1, but merely 10% of the incorporation resulted from the increase in the c9,t12 18:2 content of milk fat. Pollard et al. (16) noted that the trans-monoenoic fatty acids with a double bond at the 11th position were a much better substrate for {Delta}9-desaturase than those with a double bond at the 12th position. This is in contrast to in vitro experiments reported by Holman and Mahfouz (37) who showed that t12 18:1 was desaturated to a higher rate than t11 18:1. Interestingly, the authors assumed from their investigations that the conversion rates increased as the double bond moves away from the 9th carbon atom from the carboxyl group. Nevertheless, it is important to point out that the experimental conditions for the in vitro conversions differ from the in vivo results observed here in rats.

The reason for the observed differences in desaturation of t11 18:1 and t12 18:1 is not clear. The following 2 possibilities could be considered: 1) the t12 double bond position of t12 18:1 may possess a higher degree of steric hindrance for the {Delta}9-desaturase enzyme than the t11 double bond of t11 18:1, resulting in a lower desaturation of t12 18:1; and 2) the overall rate of desaturation is determined by the rate of activation, deacylation of the acyl-CoA complex, and acyl-transferase involved in desaturation (38). Lippel et al. (39) reported a higher activation rate for t11 18:1 than for t12 18:1, which suggests differences in the binding affinities of these 2 tFA at the catalytic site of the enzyme. This may account for the increased accumulation of t12 18:1 in rat tissues. Overall, these findings illustrate how the differences in the catalytic selectivity of acyl-CoA synthetase, {Delta}9-desaturase (isoforms), and structural confirmation lead to differences in net accumulation in rat tissues.

For rats, 2 highly homologous isoforms (SCD1 and SCD2), coding for the {Delta}9-desaturase, were characterized (40,41). Despite the fact that both isoforms are structurally similar, they exhibit divergent tissue-specific expressions (31). Some tissues also express these desaturases constitutively (42). The tissue-specific pattern of the expression for the SCD isoforms seems to be a reflection of the physiologic importance of the synthesis and/or maintenance of tissue fatty acid levels represented by the metabolic rates in the respective tissue. Data from the present study extend the above finding by demonstrating remarkable differences in the conversion rate between the tissues of the rats. For both fatty acids investigated, the conversion rates in the tissues, ranked in order of decreasing conversion efficiency, were as follows: testes = kidneys > adipose tissue > ovaries > muscle > liver > heart. This observation agrees with previous rat studies reporting small enzyme activities in liver and heart (43) and high enzyme activities in testes and kidney (44). A low conversion rate could be due to low desaturase activity as a result of deficient expression or low tissue-specific metabolic rate and vice versa. In addition, the expression profile and enzyme activity are modulated by numerous factors related to the physiologic state and dietary components (42).

The data presented here clearly indicate gender-related differences in the conversion rate. In general, higher conversion rates were found in male than in female rats, with the exception of a slightly higher conversion rate found in adipose tissue of the females. The underlying cause for the gender difference in the conversion rates of the 2 tFA is not clear, but previous findings offer possible explanations. For example, the existence of a sexually dimorphic pattern of gene expression and protein level of this enzyme was related predominantly to hormonal factors such as testosterone, estrogen, or leptin (45–48). Tissues from male and female rats have partially different metabolic functions, and the genes from different metabolic pathways are expressed in a gender-dependent manner (49). Furthermore, the observation described above might be explained by the fact that male rats have a higher metabolic rate associated with a higher growth rate.

Chin et al. (50) concluded from their investigations that the formation of c9,t11 18:2 can occur in the gut by intestinal microorganisms. The bacterial isomerization of linoleic acid (c9,c12 18:2) to c9,t11 18:2 and t11 18:1 takes place in the cecum and colon, where absorption of long-chain fatty acids is negligible (51). Therefore, the uptake of bacterially synthesized fatty acids is possible only via coprophagy (52). This appears to account for the small amounts of c9,t11 18:2 and t11 18:1 found in the control group tissues that could have been derived only from ingestion of the fecal t11 18:1 and c9,t11 18:2, and subsequent conversion of t11 18:1 to c9,t11 18:2 in the rat tissue.

The feeding of the 2 tFA isomers to rats led to marked differences in their accumulation and net metabolism. These differences in accumulation could also reflect physiologic and etiological differences between these tFA isomers. The physiologic relevance of the findings (e.g., metabolic effects and health effect) is not clear because the association between specific FA changes and risk factors is not known. It is also not known whether these animal results can be extrapolated to humans. However, it raises the need for accurate reporting of the composition of all of the different tFA isomers and encourages further research to clarify differences in the metabolism of each individual tFA isomer and identify the tFA responsible for an increased risk of coronary heart disease.


   FOOTNOTES
 
1 Presented in part at the 26th World Congress and Exhibition of ISF, September 2005, Prague, Czech Republic [Kraft J, Hoschek L, Jahreis G, Kramer JKG. Comparative conversion of c11, t11, c12, and t12 C18:1 to C18:2 fatty acids in different tissues of the animal model rat. (Poster: HUNU-39, Abstract)]. Back

2 Supported by DFG Grant JA 893. Back

4 Abbreviations used: tFA, trans fatty acid; tOIM trans octadecenoic acid isomer mixture; stearoyl-CoA desaturase, SCD. Back

Manuscript received 8 November 2005. Initial review completed 23 November 2005. Revision accepted 31 January 2006.


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 ABSTRACT
 MATERIAL AND METHODS
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 DISCUSSION
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