![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Department of Animal Science, Texas A&M University, College Station, TX 77843 and * U.S. Department of Agriculture/ARS Children’s Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030
4To whom correspondence should be addressed. E-mail: sbsmith{at}tamu.edu.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
9 desaturase index and adiposity in pigs. Early weaned piglets (n = 6/group) were fed for 35 d diets supplemented with 15 g/100 g diet beef tallow or corn oil, or 12 g/100 g tallow or corn oil plus 3 g CLA. There were no effects of dietary fat or CLA on the mass of dissected skin, bone, muscle or adipose tissue of the 7th to 9th thoracic rib sections. Medial subcutaneous adipose tissue of pigs fed tallow had smaller adipocytes than that of pigs fed corn oil. The lateral subcutaneous site was unaffected by dietary fat type. Microsomes accumulated <50% the concentration of trans-10,cis-12, cis-11,trans-13, and cis-9,trans-11 CLA as membrane and nonmembrane fractions of adipose tissue and longissimus muscle. There was no evidence of preferential incorporation of any CLA isomer into any of the subcellular fractions. Addition of CLA to the diets reduced adipose tissue nonmembrane monounsaturated fatty acids (MUFA; g/100 g total fatty acids) by 15% in corn oil–fed pigs and by 19% in tallow-fed pigs. Total saturated fatty acids (SFA) were increased by CLA commensurately in this lipid fraction. This resulted in a reduced 9 desaturase index [MUFA/(SFA + MUFA)] in the nonmembrane lipid fraction of pigs fed either the corn oil or tallow diets. Thus, in spite of marked effects on fatty acid composition and the 9 desaturase index, CLA had no effect on adiposity in early weaned piglets fed high fat diets.
KEY WORDS: • conjugated dienes • fatty acids • microsomes • adiposity • pigs
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
). Studies using mixed CLA isomers show reductions in total cholesterol, triacylglycerols and LDL in blood from humans (2
) and hamsters (3
), and decreased atherogenic plaques in rabbits (4
). CLA has exhibited additional benefits by reducing proinflammatory prostaglandin E2 levels in tissues as diverse as bone (5
) and sensitized guinea pig tracheae (6
).
The recent availability of purified CLA isomers has allowed researchers to separate the different biological effects of the two main isomers. The trans-10,cis-12 CLA isomer is associated with reduced body fat accumulation in many animal species (3
,7
–9
). Although numerous reports have pointed out the anticarcinogenic properties of mixed CLA (10
–12
), this effect can now be attributed to the cis-9,trans-11 isomer (12
), which accomplishes this without influencing adiposity (3
,8
).
The trans-10,cis-12 CLA isomer may depress adipogenesis by decreasing transcription of nuclear proteins CCAAT/enhancer binding protein 
and peroxisome proliferator-activated receptor 
(13
). These transcription factors have important regulatory roles in adipogenesis (14
–16
). CLA may also exert its effects on adiposity in various animal species by reducing activities of lipoprotein lipase (17
) and stearoyl-CoA desaturase (SCD) (7
–9
,18
), leading to smaller adipocyte cell size (19
–20
). The reduction in SCD activity supports reports of CLA-mediated decreases in adipose tissue monounsaturated fatty acids (MUFA) and concurrent increases in saturated fatty acids (SFA) in pigs (21
–23
). Other enzymes inhibited by trans-10,cis-12 CLA in mice include fatty acid synthase and acetyl-CoA carboxylase (24
). Adipocyte size could also be decreased by enhanced fatty acid oxidation. Studies in rats (25
) and mice (26
) suggest that CLA makes this possible via increased carnitine palmitoyltransferase activity. The general effect of CLA on energy metabolism has also been explored, showing increases in mice (27
–28
) and hamsters (3
), but no effect in humans (29
) or pigs (30
).
Park et al. (9
) reported that adding CLA directly to mice liver microsomal fractions directly inhibited SCD enzyme activity. This led us to hypothesize that microsomal membranes may become especially enriched in CLA. Therefore, one objective of this research was to analyze the fatty acid composition of subcutaneous adipose tissue and longissimus muscle from early weaned piglets to document the enrichment of specific CLA isomers in neutral lipids, membranes and microsomes. We previously demonstrated marked increases in SCD gene expression in postweaning pigs during a period of adipocyte hypertrophy (31
), and demonstrated recently that CLA depresses SCD enzyme activity in adipose tissue of young pigs (32
). We hypothesized that feeding CLA in the early postweaning period would enrich microsomal trans-10,cis-12 CLA, resulting in depressed SCD activity and thereby reducing adiposity.
In mice, dietary cis-9,trans-11 CLA is incorporated into neutral lipids, but does not affect incorporation of polyunsaturated fatty acids (PUFA) into neutral lipids (33
). However, Belury and Kempa-Steczko (34
) demonstrated earlier that a mixture of dietary CLA isomers was incorporated into neutral lipids at the expense of 18:2(n-6), and proposed that this may have influenced prostaglandin synthesis and consequent biological actions. Therefore, the interaction between dietary CLA and types of fatty acids (corn oil vs. beef tallow) was investigated. High levels of dietary fat (39% energy from fat) were used to mimic human diets more closely.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
This study was approved by the Baylor College of Medicine and the Texas A&M University institutional animal care committees. Pigs (n = 24) were weaned at 17 d of age and fed a basal, corn/soybean meal–based diet supplemented with (per 100 g diet): 15 g tallow; 12 g tallow + 3 g CLA; 15 g corn oil; or 12 g corn oil + 3 g CLA for 35 d. Fatty acid analysis and composition of the diets are shown in Tables 1
and 2
, respectively. The CLA source was CLA-60 provided by Conlinco (Detroit Lakes, MN). According to the manufacturer’s specifications, CLA-60 contained 60% total CLA isomers. Thus, feeding 3 g CLA/100 g diet in the 15 g/100 g treatment provided 1.8 g/100 g of the diet as CLA. Our fatty acid analysis showed that 36 g/100 g lipid of the CLA-60 oil consisted of the two major isomers known to have biological effects, cis-9,trans-11 and trans-10,cis-12 CLA (Table 1
). Pigs were fed at the USDA Children’s Nutrition Research Center in Houston, TX, with actual feed intake carefully documented. The dosage of CLA in this study was 
1230 mg/kg body, compared with 40–76 mg CLA/kg body in human dietary trials (2
,35
). Similarly, we fed 1021 mg CLA/MJ metabolizable energy (ME) intake, compared with 269 mg CLA/MJ ME in the most highly supplemented human diet (2
). The test diets contained 39% energy from fat, 20% energy from protein and 41% energy from carbohydrate.
|
|
The pigs were transported in an air-conditioned van to Texas A&M University at the end of the feeding period on d 35 and 36 and were killed humanely using standard industry techniques. Carcasses were quickly frozen and maintained at -20°C. Previously frozen pig carcasses were held at 8°C for 4 d before dissection. Rib sections containing the 7th through 9th thoracic ribs were excised and residual organ tissue trimmed away. The rib sections were carefully dissected into their major components, i.e., total muscle, total adipose tissue, total bone and total skin. Weights of these components were recorded for each animal. Specific samples of tissue were collected and frozen at -20°C for other analyses. Samples for cellularity were collected from medial subcutaneous adipose tissue overlying the spine at the 8th rib, and from lateral subcutaneous adipose tissue 2.5 cm from the distal end of the 8th rib. For the cellular lipid analysis, samples obtained were muscle from the center of the M. longissimus dorsi and subcutaneous adipose tissue overlying the spine at the 8th rib.
Cellularity.
Adipocyte size and volume were determined as described by Etherton et al. (36
) with modification by Prior (37
). Frozen adipose tissue from the two sites (medial and lateral subcutaneous) was sliced into sections 1-mm thick and placed in 20-mL scintillation vials. Tissues were rinsed three times with 37°C 0.154 mol/L NaCl at 1-h intervals to remove free lipid. After the last rinse, 0.6 mL of 50 mmol/L collidine-HCl buffer (pH 7.4) was added to each sample, followed by 1.0 mL of 3% osmium tetroxide in collidine. After incubation for 96 h at 37°C, the osmium solution was removed and the tissue rinsed three times with 0.154 mol/L NaCl until clear. Samples were incubated in 10 mL of 8 mol/L urea at 25°C for 96 h. After filtration of the fixed cells through 240-, 64- and 20-µm nylon mesh screens with 0.01% Triton in 0.154 mol/L NaCl, cells collected from the 64- and 20-µm screens were used for determination of cell size, volume and cells/g tissue, using a Model ZM Coulter Counter equipped with a Model 256 channelizer (Coulter Electronics, Hialeah, FL). Total subcutaneous adipocytes were estimated for each rib section using the mean cells/g from this analysis and total adipose tissue weight.
Analysis of cellular lipids.
Tissue samples (1 g) from an adipose tissue site (medial subcutaneous) and a muscle site (longissimus) were each separated into membrane, microsome and neutral lipid (i.e., nonmembrane) fractions by a multiple centrifugation procedure described previously (38
). Samples were homogenized in 0.1 mol/L potassium phosphate buffer (pH 7.4) using a Brinkman Polytron PT 10–35 homogenizer (Brinkman Instruments, Westbury, NY) at medium setting. Homogenates were centrifuged at 27,000 x g in a Beckman J2–21 centrifuge (Beckman Instruments, Irvine, CA) at 4°C for 30 min. The fatty supernate containing nonpolar lipids (nonmembrane fraction) was separated from the infranate cytosolic fraction, which was removed and saved, whereas the pellet (membrane) fraction (containing plasma membranes, nuclei and mitochondria) was resuspended in the same phosphate buffer and centrifuged at 27,000 x g for 30 min at 4°C. The aqueous supernates from all centrifugations were pooled and centrifuged at 105,000 x g in a Beckman L8–80 ultracentrifuge for 60 min at 4°C. The resulting supernate, containing traces of neutral lipid, was pooled with the previous nonmembrane fraction, and the nonmembrane, microsome and membrane fractions were extracted immediately for determination of fatty acid composition.
Total lipid was extracted by the method of Folch et al. (39
). After methylation (40
), the fatty acid methyl esters (FAME) were analyzed using a Varian gas chromatograph (model CP-3800 fixed with a CP-8200 autosampler, Varian Walnut Creek, CA) by the method of Sturdivant et al. (41
). Separation of FAME was accomplished on a fused silica capillary column CP-Sil88 (100 m x 0.25 mm i.d.; Chrompack Middleburg, The Netherlands). Helium was the carrier gas. After 32 min at 180°C, the oven temperature was increased at 20°C/min to 225°C and held for 13.75 min. Total run time was 48 min. Injector and detector temperatures were 270 and 300°C, respectively. Individual FAME were quantified as a the percentage of total FAME analyzed. An index of SCD enzyme activity, the 9 desaturase index, was calculated as MUFA/(SFA + MUFA) (42
).
Data analysis.
Statistical analyses were performed using the SuperAnova program (Abacus Concepts, Berkeley, CA). One-way ANOVA was used to analyze the main effects of diet on tissue differences (adipose or muscle) and subcellular component (membrane, microsome or nonmembrane). For all other measures, a two-way ANOVA was performed, with the basal dietary fat (corn oil or tallow) as factor one, and the absence or presence of supplementary CLA as factor two. Fisher’s Least Squared Means test was used to separate means. Effects were considered significant at P < 0.05.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
There were no effects of fat (corn oil vs. tallow) or CLA or a fat x CLA interaction for final weight, daily gain or feed intake (data not shown). The gain:feed ratio was greater in corn oil–fed pigs than in tallow-fed pigs (0.65 ± 0.01 vs. 0.61 ± 0.01, respectively). There were no fat, CLA or fat x CLA interactions for the components of the 7th through 9th thoracic rib section (Table 3
). This was true when the data were expressed as absolute mass or as a percentage of rib section mass.
|
There were no effects of dietary fat or CLA or a fat x CLA interaction for adiposity of the lateral subcutaneous adipose tissue site (Table 4
). Pigs fed the tallow diet had more cells/100 mg adipose tissue and therefore more total adipocytes per 7th through 9th rib section than those fed corn oil (medial plus lateral sites combined). There was a greater proportion of larger adipocytes in medial subcutaneous adipose tissue from pigs fed corn oil than in adipose tissue from pigs fed tallow, regardless of the presence of CLA in the diet (Fig. 1
; data pooled across CLA treatments). CLA had no effect on adipocytes/100 mg adipose tissue or on adipoctye volume.
|
|
|
Fatty acid composition |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
Main effects for subcellular fraction were significant for all fatty acids (data not shown). Microsomes contained lower concentrations of MUFA (except 14:1), PUFA [except 20:4(n-6)] and CLA isomers, and contained more SFA than membrane and nonmembrane fractions. The nonmembrane fraction contained the lowest concentration of 14:1 and 20:4(n-6). With the exception of 14:1 and 20:4(n-6) (which both were higher in membranes), membrane and nonmembrane fatty acid concentrations were the same. Main effects for tissue (muscle vs. adipose tissue) were significant for all fatty acids except 18:0. Muscle contained smaller concentrations of all MUFA except 14:1, less PUFA except 20:4(n-6) and more SFA than adipose tissue. Muscle contained more cis-9,trans-11 CLA than adipose tissue, but less cis-11,trans-13 and trans-10,cis-12 CLA than adipose tissue. The 9 desaturase index was lower in CLA-fed pigs than in pigs not fed CLA (0.36 vs 0.43; pooled SEM = 0.018, P = 0.001).
Membrane fatty acid composition.
The concentrations of SFA and MUFA were greater in membranes of tallow-fed pigs, whereas PUFA were greater in membranes of corn oil–fed pigs (Table 5
). CLA had no effect on adipose tissue membrane fatty acids, but decreased 16:1 by 10–18% and 18:1 by 15–18% in muscle membranes. CLA decreased 18:2(n-6) by 10% in adipose tissue membranes from corn oil–fed pigs, but had no effect in adipose tissue membranes from tallow-fed pigs. The dietary fat x CLA interaction was significant for the concentrations of CLA isomers in muscle membranes; there was a greater increase in all CLA isomers in muscle membranes of corn oil–fed pigs than in membranes from tallow-fed pigs in response to the supplementary CLA (Table 5
). In adipose tissue, cis-9,trans-11 CLA was higher in membranes of tallow-fed pigs than in membranes of corn oil–fed pigs. CLA decreased the 9 desaturase index in muscle, but not adipose tissue membranes.
|
Dietary CLA increased all CLA isomers in adipose tissue and muscle microsomes (Table 6
), although the concentrations were < 50% of those in membrane (Table 5
) or nonmembrane fractions (Table 7
). In adipose tissue microsomes, dietary tallow increased 16:1 and 18:1, whereas dietary CLA decreased the concentrations of both monounsaturates. The concentration of 18:2(n-6) was greater in adipose tissue microsomes of pigs fed corn oil than in those of tallow-fed pigs. In muscle microsomes, 14:1 and 16:1 were greater in tallow-fed pigs, whereas 18:2(n-6) was greater in corn oil–fed pigs. Dietary CLA reduced the concentration of total microsomal MUFA, but had no effect on the 9 desaturase index in microsomes from either tissue (Table 6
).
|
|
All SFA and MUFA concentrations were greater in adipose tissue nonmembrane lipids from pigs fed tallow, whereas PUFA concentrations were greater in nonmembrane lipids of corn oil–fed pigs (Table 7
). The concentration of cis-9,trans-11 CLA was higher in adipose tissue nonmembrane lipids of pigs fed tallow than in those of pigs fed corn oil. In adipose tissue nonmembrane lipids, CLA affected the concentrations of all fatty acids except 14:1 and 16:0; SFA and CLA concentrations were increased, whereas MUFA and PUFA concentrations were decreased by supplementary CLA. The 9 desaturase index was higher in adipose tissue nonmembrane lipids of corn oil–fed pigs than in tallow-fed pigs, and was depressed by CLA. CLA decreased 16:1 and 18:1 in muscle nonmembrane lipids, but the 9 desaturase index was unaffected by fat type or CLA (Table 7
).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
9 desaturase index, which we predicted would be related to a reduction in lipid filling of adipocytes. Although research in several species has indicated that CLA can reduce adipose tissue accumulation (3
,7
–9
), we were unable to demonstrate this effect in piglets fed diets high in fat (>18 g/100 g; sum of basal and supplemental dietary fat) compared with typical production diets (3–4 g/100 g). We also demonstrated no effect of 1.5 g CLA/100 g diet on adiposity in pigs fed identical corn/soybean basal diets (32
). Thus, it has not been possible for us to replicate the effects of CLA on adiposity using early weaned piglets. Although the rib dissection measurements in the present study indicated no difference in subcutaneous adipose tissue mass, the pigs fed the tallow diets with and without CLA had significantly more estimated total adipocytes than the corn oil–fed pigs. A major contributor to this effect was the much larger numbers of smaller adipocytes at the medial site in tallow-fed piglets. Additionally, the corn oil–fed pigs had greater distributions of larger volume adipocytes at the medial site. Thus, our measure of rib section adiposity was sufficiently sensitive to detect dietary effects. Clearly, CLA had no effect on either total adipose tissue mass or adipocyte number in the thoracic rib section of young, weanling piglets.
The high percentage of dietary fat in the basal diets (12 g added fat/100 g diet) potentially diluted CLA isomer concentrations and eliminated their effects on adiposity. Previous investigations feeding CLA to pigs focused primarily on improving animal products, and CLA was added to standard swine diets containing 3–4 g lipid/100 g diet (43
–46
). Had the dilution of CLA been the reason for the lack of changes in body composition in the current study, the tissue content of CLA isomers would have been low compared with previously published results. To the contrary, the total of the three major CLA isomers in adipose tissue nonmembrane lipids constituted 4.78 g/100 g fatty acids for pigs fed corn oil + CLA and 5.18 g/100 g fatty acids for pigs fed tallow + CLA. In longissimus muscle nonmembrane lipids, the three CLA isomers totaled 2.73 g/100 g fatty acids for pigs fed corn oil + CLA and 2.30 g/100 g fatty acids for pigs fed tallow + CLA. These figures compared favorably to previous research with pigs that demonstrated significant reductions in adiposity (43
–46
). However, the previous research was with market-weight pigs rather than with early weaned piglets. Thus, the age at which pigs are exposed to CLA may dictate the efficacy of CLA in reducing adiposity.
This investigation demonstrated that microsomal membranes less effectively incorporated the CLA isomers. Although dietary CLA enriched microsomal CLA isomers, concentrations of CLA isomers were <50% of those observed in the other cellular components. The membrane fraction contained the cellular membranes (with associated connective tissues) and mitochondrial membranes, whereas the nonmembrane fraction contained neutral lipids and any phospholipids that may have dissociated from membranes during the extraction process. Kramer et al. (47
) demonstrated that, relative to dietary isomers, CLA cis-9,trans-11 was enriched, whereas CLA trans-10,cis-12 was at a lower concentration, in hepatic phospholipids of pigs fed 2% CLA from 61.5 to 106 kg live weight. We saw no evidence for preferential enrichment of the membrane or microsomal fractions with any of the isomers of CLA we quantified.
The 9 desaturase index is calculated as MUFA/(MUFA + SFA) (42
), and this index was significantly lower in CLA-fed pigs (0.36 vs. 0.43 in pigs not fed CLA; data pooled across tissues and subcellular fractions). Although the main effect was significant, the only tissue fractions in which the 9 desaturase index was depressed significantly by CLA were adipose tissue nonmembrane lipids and muscle membranes. Adipose tissue nonmembrane lipid is composed primarily of triacylglycerols, and the fatty acid composition of this fraction is dictated both by endogenous synthesis of fatty acids as well as dietary fatty acid composition. CLA increased SFA and decreased MUFA in nonmembrane lipids. This would occur only if the microsomal SCD enzyme activity were depressed, leading to reduced incorporation of MUFA into triacylglycerols. It is unusual that the 9 desaturase index was greater in pigs fed the corn oil–based diets than in those fed the tallow-based diets, which would suggest that dietary tallow depressed, or corn oil stimulated SCD enzyme activity. This is inconsistent with previous studies in pigs (48
), rats (49
) and dogs (50
).
In a separate study (32
), we demonstrated that feeding 1.5 g CLA/100 g diet to early weaned pigs reduced the 9 desaturase index to 0.36, which was significantly lower than the indices observed in pigs fed 1.5 g corn oil/100 g diet (0.53) or 1.5 g beef tallow/100 g diet (0.54; pooled SEM = 0.02). Thus, corn oil had no effect on the 9 desaturase index in our previous investigation, unlike the results in this study. The corn oil–based diets of this study had higher MUFA:SFA ratios than the tallow-based diets, and this was reflected in the MUFA and SFA composition of the adipose tissue nonmembrane lipids. However, the addition of CLA to the diets actually increased the MUFA:SFA ratio in both the corn oil–based diet (1.93 vs. 1.85) and the tallow-based diets (1.35 vs. 1.15). Thus, the depression of the 9 desaturase index by CLA was caused by a reduction in the conversion of SFA to their respective MUFA. We conclude that the 9 desaturase index adequately predicts the effects of CLA on SCD enzyme activity, but is not an effective estimator of SCD enzyme activity for comparisons of diets that differ widely in fatty acid composition.
Finally, we had predicted that CLA would reduce lipid filling of adipocytes in these early weaned piglets. However, the reduction in the 9 desaturase index demonstrated in this study in adipose tissue nonmembrane lipids was not associated with a reduction in adipocyte volume. The greater adipocyte volume in pigs fed 15 g corn oil/100 g diet indicated that it was possible to affect adipocyte volume by dietary means, consistent with our previous investigations in postweaning pigs (51
). These and our previous results (32
) suggest that, if SCD activity is required for adipocyte lipid filling, then sufficient activity remained in the CLA-fed pigs to support this process.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
2 Funded in part with federal funds from the USDA, ARS under Cooperative Agreement no. 58–6250-1–003.
3 The contents of this publication do not necessarily reflect the views or policies of the USDA, nor does mention of trade names, commercial products, or organizations imply endorsement from the U. S. Government.
5 Abbreviations used: CLA, conjugated linoleic acid; FAME, fatty acid methyl esters; ME, metabolizable energy; MUFA, monounsaturated fatty acids; PUFA, polyunsaturated fatty acids; SCD, stearoyl-CoA desaturase; SFA, saturated fatty acids.
Manuscript received 6 March 2002. Initial review completed 26 April 2002. Revision accepted 15 August 2002.
|
LITERATURE CITED |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSFatty acid compositionDISCUSSIONLITERATURE CITED |
|---|
1. Pariza, M. W., Park, Y. & Cook, M. E. (2000) Mechanisms of action of conjugated linoleic acid: evidence and speculation. Proc. Soc. Exp. Biol. Med. 223:8-13.
2. Blankson, H., Stakkestad, J. A., Fagertun, H., Thom, E., Wadstein, J. & Gudmundsen, O. (2000) Conjugated linoleic acid reduces body fat mass in overweight and obese humans. J. Nutr. 130:2943-2948.
3. Gavino, V. C., Gavino, G., Leblanc, M. J. & Tuchweber, B. (2000) An isomeric mixture of conjugated linoleic acids but not pure cis-9,trans-11-octadecadienoic acid affects body weight gain and plasma lipids in hamsters. J. Nutr. 130:27-29.
4. Kritchevsky, D., Tepper, S. A., Wright, S., Tso, P. & Czarnecki, S. K. (2000) Influence of conjugated linoleic acid (CLA) on establishment and progression of atherosclerosis in rabbits. J. Am. Coll. Nutr. 19:472S-477S.
5. Li, Y. & Watkins, B. A. (1998) Conjugated linoleic acids alter bone fatty acid composition and reduce ex vivo prostaglandin E2 biosynthesis in rats fed n-6 or n-3 fatty acids. Lipids 33:417-425.[Medline]
6. Whigham, L. D., Cook, E. B., Stahl, J. L., Saban, R., Bjorling, D. E., Pariza, M. W. & Cook, M. E. (2001) CLA reduces antigen-induced histamine and PGE(2) release from sensitized guinea pig tracheae. Am. J. Physiol. 280:R908-R912.
7. Baumgard, L. H., Corl, B. A., Dwyer, D. A., Saebo, A. & Bauman, D. E. (2000) Identification of the conjugated linoleic acid isomer that inhibits milk fat synthesis. Am. J. Physiol. 278:R179-R184.
8. Choi, Y. J., Kim, Y. C., Han, Y. B., Park, Y., Pariza, M. W. & Ntambi, J. M. (2000) The trans-10,cis-12 isomer of conjugated linoleic acid downregulates stearoyl-CoA desaturase 1 gene expression in 3T3–L1 adipocytes. J. Nutr. 130:1920-1924.
9. Park, Y., Storkson, J. M., Ntambi, J. M., Cook, M. E., Sih, C. J. & Pariza, M. W. (2000) Inhibition of hepatic stearoyl-CoA desaturase activity by trans-10,cis-12 conjugated linoleic acid and its derivatives. Biochim. Biophys. Acta 1486:285-292.[Medline]
10. Hubbard, N. E., Lim, D., Summers, L. & Erickson, K. L. (2000) Reduction of murine mammary tumor metastasis by conjugated linoleic acid. Cancer Lett 150:93-100.[Medline]
11. Liu, K. L. & Belury, M. (1998) Conjugated linoleic acid reduces arachidonic acid content and PGE2 synthesis in murine keratinocytes. Cancer Lett. 127:15-22.[Medline]
12. O’Shea, M., Devery, R., Lawless, F., Murphy, J. & Stanton, C. (2000) Milk fat conjugated linoleic acid (CLA) inhibits growth of human mammary MCF-7 cancer cells. Anticancer Res 20:3591-3601.[Medline]
13. Brodie, A. E., Manning, V. A., Ferguson, K. R., Jewell, D. E. & Hu, C. Y. (1999) Conjugated linoleic acid inhibits differentiation of pre- and postconfluent 3T3–L1 preadipocytes but inhibits cell proliferation only in preconfluent cells. J. Nutr. 129:602-606.
14. Darlington, G. J., Ross, S. E. & MacDougald, O. A. (1998) The role of C/EBP genes in adipocyte differentiation. J. Biol. Chem. 273:30057-30060.
15. Mandrup, S. & Lane, M. D. (1997) Regulating adipogenesis. J. Biol. Chem. 272:5367-5370.
16. Wu, Z., Xie, Y., Bucher, N. L. R. & Farmer, S. R. (1995) Conditional ectopic expression of C/EBP in NIH-3T3 cells induces PPAR and stimulates adipogenesis. Genes Dev 9:2350-2363.
17. Park, Y., Albright, K. J., Storkson, J. M., Liu, W., Cook, M. E. & Pariza, M. W. (1999) Changes in body composition in mice during feeding and withdrawal of conjugated linoleic acid. Lipids 34:243-248.[Medline]
18. Lee, K. N., Pariza, M. W. & Ntambi, J. M. (1998) Conjugated linoleic acid decreases hepatic stearoyl-CoA desaturase mRNA expression. Biochem. Biophys. Res. Commun. 248:817-821.[Medline]
19. Azain, M. J., Hausman, D. B., Sisk, M. B., Flatt, W. P. & Jewell, D. E. (2000) Dietary conjugated linoleic acid reduces rat adipose tissue cell size rather than cell number. J. Nutr. 130:1548-1554.
20. Evans, M., Geigerman, C., Cook, J., Curtis, L., Kuebler, B. & McIntosh, M. (2000) Conjugated linoleic acid suppresses triglyceride accumulation and induces apoptosis in 3T3–L1 preadipocytes. Lipids 35:899-910.[Medline]
21. Bee, G. (2000) Dietary conjugated linoleic acids alter adipose tissue and milk lipids of pregnant and lactating sows. J. Nutr. 130:2292-2298.
22. Bee, G. (2000) Dietary conjugated linoleic acid consumption during pregnancy and lactation influences growth and tissue composition in weaned pigs. J. Nutr. 130:2981-2989.
23. Muller, H. L., Kirchgessner, M., Roth, F. X. & Stangl, G. I. (2000) Effect of conjugated linoleic acid on energy metabolism in growing-finishing pigs. J. Anim. Physiol. Anim. Nutr. 83:85-94.
24. Tsuboyama-Kasaoka, N., Takahashi, M., Tanemura, K., Kim, H. J., Tange, T., Okuyama, H., Kasai, M., Ikemoto, S. & Ezaki, O. (2000) Conjugated linoleic acid supplementation reduces adipose tissue by apoptosis and develops lipodystrophy in mice. Diabetes 49:1534-1542.[Abstract]
25. Martin, J. C., Gregoire, S., Siess, M. H., Genty, M., Chardigny, J. M., Berdeaux, O., Juaneda, P. & Sébédio, J.-L. (2000) Effects of conjugated linoleic acid isomers on lipid-metabolizing enzymes in male rats. Lipids 35:91-98.[Medline]
26. Park, Y., Albright, K. J., Liu, W., Storkson, J. M., Cook, M. E. & Pariza, M. W. (1997) Effect of conjugated linoleic acid on body composition in mice. Lipids 32:853-858.[Medline]
27. DeLany, J. P., Blohm, F., Truett, A. A., Scimeca, J. A. & West, D. B. (1999) Conjugated linoleic acid (CLA) significantly and rapidly reduces body fat content in the mouse without affecting energy intake. Am. J. Physiol. 276:R1172-R1179.
28. West, D. B., Blohm, F. Y., Truett, A. A. & Delany, J. P. (2000) Conjugated linoleic acid persistently increases total energy expenditure in AKR/J mice without increasing uncoupling protein gene expression. J. Nutr. 130:2471-2477.
29. Zambell, K. L., Keim, N. L., Van Loan, M. D., Gale, B., Benito, P., Kelley, D. S. & Nelson, G. J. (2000) Conjugated linoleic acid supplementation in humans: effects on body composition and energy expenditure. Lipids 35:777-782.[Medline]
30. Muller, H. L., Stangl, G. I. & Kirchgessner, M. (1999) Energy balance of conjugated linoleic acid-treated pigs. J. Anim. Physiol. Anim. Nutr. 81:150-156.
31. Smith, S. B., Mersmann, H. J., Smith, E. O. & Britain, K. G. (1999) Stearoyl coenzyme A desaturase gene expression during growth in adipose tissue from obese and crossbred pigs. J. Anim. Sci. 77:1710-1716.
32. Smith, S. B., Hively, T. S., Cortese, G. M., Han, J. J., Chung, K. Y., Castenada, P., Gilbert, C. D., Adams, V. L. & Mersmann, H. J. (2002) Conjugated linoleic acid depresses the 9 desaturase index and stearoyl coenzyme A desaturase enzyme activity in porcine subcutaneous adipose tissue. J. Anim. Sci. 80:2110-2115.
33. Banni, S., Carta, G., Angioni, E., Murru, E., Scanu, P., Melis, M. P., Bauman, D. E., Fischer, S. M. & Ip, C. (2001) Distributions of conjugated linoleic acid and metabolites in different lipid fractions of rat liver. J. Lipid Res. 42:1056-1061.
34. Belury, M. A. & Kempa-Steczko, A. (1997) Conjugated linoleic acid modulates hepatic lipid composition in mice. Lipids 32:199-204.[Medline]
35. Riserus, U., Berglund, L. & Vessby, B. (2001) Conjugated linoleic acid (CLA) reduced abdominal adipose tissue in obese middle-aged men with signs of the metabolic syndrome: a randomized controlled trial. Int. J. Obes. Relat. Disord. 25:1129-1135.
36. Etherton, T. D., Thompson, E. H. & Allen, C. E. (1977) Improved techniques for studies of cellularity and metabolism. J. Lipid Res. 18:552-557.[Abstract]
37. Prior, R. L. (1983) Lipogenesis and adipose tissue cellularity in steers switched from alfalfa hay to high concentrate diets. J. Anim. Sci. 56:483-489.
38. Hoelscher, L. M., Savell, J. W., Smith, S. B. & Cross, H. R. (1988) Subcellular distribution of cholesterol within muscle and adipose tissues of beef loin steaks. J. Food Sci. 53:718-722.
39. Folch, J. M., Lees, M. & Sloane-Stanley, G. H. (1957) A simple method for the isolation and purification of total lipids from animal tissues. J. Biol. Chem. 226:497-505.
40. Morrison, W. R. & Smith, L. M. (1964) Preparation of fatty acid methyl esters and dimethylacteals from lipides with boron flouride-methanol. J. Lipid Res. 5:600-607.[Abstract]
41. Sturdivant, C. A., Lunt, D. K., Smith, G. C. & Smith, S. B. (1992) Fatty acid composition of subcutaneous and intramuscular adipose tissues and M. longissimus dorsi of Wagyu cattle. Meat Sci. 32:449-458.
42. Corl, B. A., Baumgard, L. H., Dwyer, D. A., Griinari, J. M., Phillips, B. S. & Bauman, D. E. (2001) The role of 9-desaturase in the production of cis- 9, trans-11 CLA. J. Nutr. Biochem. 12:622-630.[Medline]
43. Dugan, M. E. R., Aalhus, J. L., Schaefer, A. L. & Kramer, J.K.G. (1997) The effect of conjugated linoleic acid on fat to lean repartitioning and feed conversion in pigs. Can. J. Anim. Sci. 77:723-725.
44. Ostrowska, E., Muralitharan, M., Cross, R. F., Bauman, D. E. & Dunshea, F. R. (1999) Dietary conjugated linoleic acids increase lean tissue and decrease fat deposition in growing pigs. J. Nutr. 129:2037-2042.
45. Thiel-Cooper, R. L., Parish, F. C., Sparks, J. C., Wiegand, B. R. & Ewan, R. C. (2001) Conjugated linoleic acid changes swine performance and carcass composition. J. Anim. Sci. 79:1821-1828.
46. Wiegand, B. R., Sparks, J. C., Parish, F. C. & Zimmerman, D. R. (2002) Duration of feeding conjugated linoleic acid influences growth performance, carcass traits, and meat quality of finishing barrows. J. Anim. Sci. 80:637-643.
47. Kramer, J.K.G., Sehat, N., Dugan, M. E. R., Mossaba, M. M., Yurawecz, M. P., Roach, J.A.G., Eulitz, K., Aalhus, J. L., Schaefer, A. L. & Ku, Y. (1998) Distributions of conjugated linoleic acid (CLA) isomers in tissue lipid classes of pigs fed a commercial CLA mixture determined by gas chromatography and silver-ion high-performance liquid chromatography. Lipids 33:549-558.[Medline]
48. Klingenberg, I. L., Knabe, D. A. & Smith, S. B. (1995) Lipid metabolism in pigs fed beef tallow or high-oleic acid sunflower oil. Comp. Biochem. Physiol. 110B:183-192.
49. Garg, M. L., Wierzbicki, A. A., Thompson, A.B.R. & Clandinin, M. T. (1988) Dietary cholesterol and/or n-3 fatty acid modulate 9-desaturase activity in rat liver microsomes. Biochim. Biophys. Acta 962:330-336.[Medline]
50. Giron, M. D., Mataix, F. J., Faus, M. J. & Suarez, M. D. (1989) Effect of long-term feeding olive oil and sunflower oils on fatty acid composition and desaturation activities of liver microsomes. Biochem. Int. 19:645-656.[Medline]
51. Smith, D. R., Knabe, D. A. & Smith, S. B. (1996) Depression of lipogenesis in swine adipose tissue by specific dietary fatty acids. J. Anim. Sci. 74:975-983.[Abstract]
This article has been cited by other articles:
|
|
 |
|
  I. Fernandez-Figares, J. A. Conde-Aguilera, R. Nieto, M. Lachica, and J. F. Aguilera Synergistic effects of betaine and conjugated linoleic acid on the growth and carcass composition of growing Iberian pigs J Anim Sci, January 1, 2008; 86(1): 102 - 111. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Wynn, Z. C. T. R. Daniel, C. L. Flux, J. Craigon, A. M. Salter, and P. J. Buttery Effect of feeding rumen-protected conjugated linoleic acid on carcass characteristics and fatty acid composition of sheep tissues J Anim Sci, December 1, 2006; 84(12): 3440 - 3450. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. L. Burr, C. G. Taylor, and H. A. Weiler Dietary Conjugated Linoleic Acid Does Not Adversely Affect Bone Mass in Obese fa/fa or Lean Zucker Rats. Experimental Biology and Medicine, November 1, 2006; 231(10): 1602 - 1609. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. P. Mirand, M.-A. Arnal-Bagnard, L. Mosoni, Y. Faulconnier, J.-M. Chardigny, and Y. Chilliard Cis-9, Trans-11 and Trans-10, Cis-12 Conjugated Linoleic Acid Isomers Do Not Modify Body Composition in Adult Sedentary or Exercised Rats J. Nutr., September 1, 2004; 134(9): 2263 - 2269. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Dugan, J. L Aalhus, and J. K. Kramer Conjugated linoleic acid pork research Am. J. Clinical Nutrition, June 1, 2004; 79(6): 1212S - 1216S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. H. Terpstra Effect of conjugated linoleic acid on body composition and plasma lipids in humans: an overview of the literature Am. J. Clinical Nutrition, March 1, 2004; 79(3): 352 - 361. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
