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1
*
Unité Mixte de Recherche Institut National de la Recherche Agronomique/INA, Physiologie de la Nutrition et du Comportement Alimentaire, Paris, France;
Laboratoire de Physiologie de la Nutrition, Université Paris-Sud, Orsay, France; and
**
Institut Curie, Université Paris-Sud, Orsay, France
1To whom correspondence should be addressed. E-mail: jean-charles.martin{at}ibaic.u-psud.fr.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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60% of VO2max were measured. Carnitine palmitoyltransferase-I (CPT-I), leptin, insulin and triiodothyronine concentrations, as well as the in vivo overall adiposity changes were also determined. After 6 wk, the whole-body triglyceride content determined in vivo by NMR was significantly higher in the R group than in the control and CLA mix groups. The CLA mix group differed from the others in the lack of body triglyceride accumulation between d 21 and d 45 of the study, and the appearance of a slight insulin-resistance (homeostatic model assessment index, P < 0.05). Paradoxically, the lack of effect on whole-body lipid oxidation was associated with a greater CPT-I-specific activity in tissues of both CLA-fed groups (P < 0.05). No other major effects of CLA feeding were detected. In conclusion, CLA supplementation in hamsters did not affect adipose weight or the components of energy expenditure despite a theoretically higher capacity of red muscle to oxidize lipids. Only a CLA mixture prevented whole-body triglyceride accumulation over time.
KEY WORDS: • fat mass • energy expenditure • conjugated linoleic acid isomers • nuclear magnetic resonance
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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), where it constitutes the main dietary source for humans (2
). Alternatively, the 9c,11t-isomer can be produced by 
-9 desaturation of dietary trans-vaccenic acid (trans-C18:111) (3
-5
). CLA have been receiving much attention in the past decade because of their pleiotropic biological activities. For instance, these fatty acids are effective anticarcinogens, antiatherosclerotic agents and potent modulators of immune function (6
–9
). A reduction in body fat mass and a gain in lean body mass have also been often observed in growing animals, obese humans and long-term exercising men (10
–16
) (range of CLA intake: 1.5–6% of energy). Several mechanisms have been proposed to explain part of these changes in body composition, such as an increased apoptosis of adipose cells (17
,18
), a reduced adipocyte size (19
), lower energy intake or greater energy expenditure (13
,20
–22
), and decreased fatty acid uptake by adipose tissue (23
). It should be emphasized that comparisons among studies on the effect of CLA on body fat in rodents, pigs or humans have sometimes led to contradictory conclusions. These discrepancies might originate from differences in any of the combinations of the amount and quality of the CLA mixture, gender, age, duration of supplementation or species responsiveness. Several experiments designed to measure energy expenditure have led also to contradictory results. For instance, no effects on resting energy metabolism were observed in female Sprague-Dawley rats (19
), German landrace sows (24
), or adult women (25
), whereas male AKR/J mice had increased resting energy expenditure (13
,21
,26
). But more importantly, a better understanding of the effect of CLA on energy metabolism would require examining simultaneously the various components of energy expenditure, together with humoral, biochemical and metabolic variables that may influence its intensity. In this study, we measured and compared the effect of a diet augmented with the naturally more abundant isomer, i.e., the 9c, 11t-isomer, with that of a commercial mixture of CLA with equal amounts of the 9c,11t-isomer and the 10t,12c-isomer, on basal energy expenditure, metabolic response to feeding, spontaneous activity, treadmill running at moderate intensity (60% of the maximal aerobic power for 2 h) and during the postexercise recovery period (for 3 h after completion of the run) in growing-finishing hamsters. In addition, the specific oxidation of glucose and lipid during these periods were computed from oxygen consumption and carbon dioxide release. We also evaluated the effects of the CLA-containing diets on several endocrine and biochemical responses, body composition, and protein accumulation into liver and muscle from dietary proteins. |
MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Official French regulations (87848) for the care and use of laboratory animals were followed (03056). Male hamsters, bred in our animal facility (LPN strain) were housed 10 per cage in plastic cages (with a wire bottom positioned 1.5 cm above the floor to prevent as much as possible coprophagia and wood dust ingestion), in a controlled environment, with constant temperature (22°C ± 1) and humidity (70%), and an artificial light-dark cycle (dark from 1930 h to 0730 h). They were fed a standard nonpurified diet AO4 (UAR Villemoisson-sur-Orge, Epinay-sur-Orge, France) until 7 wk of age. Then they were fed a purified diet containing (in energy) 48.9% carbohydrate, 17.9% casein, and 32.9% lipid (Table 1
) for 2 wk before the experimental dietary period. The nutritional adequacy of the diet has been evaluated elsewhere (27
). The hamsters were then housed individually and assigned to one of 3 diets: 1) the standard diet (control group); 2) the standard diet augmented with 9c,11t-isomer to 1.6% (in energy); or 3) the standard diet augmented with a CLA mixture to 3.2% (in energy; see isomeric CLA distribution below). We assumed an energy equivalent of 37.6 kJ/g of CLA. CLA was added to the basal diet with no substitution for carbohydrate, fat or protein. The 9c,11t-isomer (81.5% pure) was synthesized from dehydrated castor oil as previously described (28
). The fatty acid composition (g/100 g) was as follows: 9c,12t-18:2, 5.8; 9c,12c-18:2, 2; 9c,11t-18:2, 81.5; 9c,11c-18:2, 7.5; and 9t,11t-18:2, 1.8. The CLA mixture (78.2% pure) was kindly donated by Seah International (Boulogne sur mer, France) and contained: 16:0, 4.2; 18:0, 1.5; 9c-18:1, 12.5; 11c-18:1, 0.6; 9c, 12t-18:2, 0.2; 9t,12c-18:2(n-6), 0.1; 9c12c-18:2, 2.1; all 8,10–18:2 isomers, 0.8; all 7,9–18:2 isomers, 0.7; all 11,13–18:2 isomers, 0.4; all 12,14–18:2 isomers, 0.1; 10c,12c-18:2, 0.6; 9c,11c-18:2, 0.8; 9c,11t-18:2, 37.2; 10t, 12c-18:2, 38 (i.e., CLA isomeric repartition was 47.2% 9c11t-, 48.2% 10t,12c-, and 4.6% for the other CLA isomers). The fatty acid composition was determined by gas chromatography/mass spectrometry on methyl-triazoline dione adducts (for CLA isomer determination), completed by gas chromatographic analysis of fatty acid methyl esters (FAME), and additionally checked by one column silver-nitrate HPLC carried out on FAME. Determination of the total CLA content of the based diet was made by a combination of reversed-phase HPLC and gas chromatography using only FAME (29
). The total CLA in the fat of the basal-diet was 0.45 g/100 g total fatty acids, and the isomeric distribution can be tentatively given as (g/100 g total fatty acids): 9c,11t + 8t,10c, 0.28; 9t,11c, 0.015; 10t, 12c, 0.009; all ciscis-isomers, 0.067; 11t, 13t, 0.019; other transtrans-isomers, 0.064.
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15N atom enrichment) was obtained from 15N-labeled milk by giving an oral dose of 50 g/d of (15NH4)2SO4 (10 atom % isotope enrichment; Euriso-top, Saint Aubin, France) to a lactating cow for 11 d (30
). 15N atom enrichment was measured in liver and muscle tissue (hind limb) as an indicator of dietary amino acid incorporation into body tissues. Body weight gain and food intake.
Body weight was measured twice weekly and food intake was measured daily at the end of the dark period.
Measurement of the components of energy expenditure by indirect calorimetry.
To measure the effect of the treatments on components of energy expenditure, hamsters were housed for 24 h in a metabolic chamber connected to an opened-circuit indirect calorimetry system (31
).
Because of the low metabolic rate of such small animals, the measurements were done on pairs of hamsters housed together in the metabolic cage so as to provide a stronger metabolic signal. Air flow through the metabolic cage was adjusted at 1.5 L/min by a flow controller-mass flow meter. Oxygen consumption (VO2) and carbon dioxide production (VCO2) were recorded every 10 s by means of a computer-assisted program of data acquisition. Spontaneous activity was also recorded quantitatively by means of piezo electric strain gauges (sensitivity 0.1 g) located beneath the metabolic cage. Computer-assisted processing of the respiratory exchanges and spontaneous activity signals allowed us to compute the part of total metabolic rate (TMR) devoted to spontaneous motion (Mact) (31
,32
). By subtracting Mact from TMR, it was possible to compute continuously resting metabolism, a component that we call background metabolic rate (BgM) (31
). BgM differs from the true resting metabolism, which in metabolic devices can be measured only when the animal stays motionless for at least 15–30 min. Two articles have been published that describe in detail the functioning of the system and the processing of the data (31
,32
).
The night preceding the calorimetric experiment, the hamsters were allotted only one-half of their spontaneous food intake to be in a postabsorptive state the next morning. They were housed in the metabolic cage at 1000 h with no food available but free access to water. At 1500 h, two food cups containing a calibrated test meal (2 x 1.5 g of the usual diet) were introduced in the cage. (The use of two separate food cups prevented competition between the hamsters so that each of them ingested 1.5 g of food.) Data acquisition was continued until the next day at 0900 h.
In this experiment the various components contributing to overall total energy expenditure were computed after the metabolic values were expressed per kg body(0.75).
The respective oxidations of carbohydrates and lipids associated with BM, TEF and Mact were computed form VO2 and VCO2 using standard stoichiometric formulae (31
,33
), assuming that the rate of protein oxidation was constant and amounted to the daily dietary protein intake, i.e., 1 mg/min (0.5 mg/min in each hamster).
Measurement of energy metabolism during treadmill running (expt. B).
Respiratory exchanges were measured on pairs of hamsters running on a 10% slope in a home-made airtight treadmill connected to the metabolic device already used in the previous study. The exercise was chosen to be of long duration and moderate intensity to favor a metabolic state in which both carbohydrates and lipids would participate in energy expenditure (34
).
Airflow through the treadmill was increased from 1.5 L/min to 2.5 L/min to take into account the increased energy expenditure during running and data acquisition was started at 0900 immediately after the hamsters were put on the treadmill. The hamsters were allowed to rest on the treadmill belt for 2 h before the onset of exercise to permit recording of pre-exercise resting values of metabolism and substrate oxidation. Exercise per se was started at 1100 h. After a 10-min warmup at 10 m/min, the speed of the treadmill was set at 18 m/min (65% of the VO2 max of 27 m/min) and maintained constant until 1300 h. The measurement of the respiratory exchanges was continued until 1600 h to study also postexercise metabolism and substrate oxidation. As in the previous study, protein oxidation was assumed to be constant at 1 mg/min and metabolic values were adjusted per kilogram body(0.75).
Tissue removal and blood sampling for hormonal determination.
The hamsters were deeply anesthetized with Zoletil 50 (250 mg/kg; Tiletamine chlorohydrate, Zolazepam chlorohydrate, 50:50, wt/wt; Reading Laboratory, Nice, France) immediately after the measurements in the calorimetric device (expt. A) or after 2–5 d of recovery from the exercise and 18 h of food deprivation (expt. B).
Blood samples were taken by cardiac puncture in the hamsters of experiment B, between 900 and 1000 h in the morning. Two hundred fifty microliters of blood was taken in a first puncture 
2 min after anesthesia. Ten microliters of blood was immediately used for measurement of glucose. The plasma of the remaining blood was then separated by centrifugation (4°C, 20 min, 3000 x g) and stored at -80°C for further determination of insulin. Two milliliters of blood was collected from a second puncture. The plasma was immediately separated by centrifugation (4°C, 20 min, 3000 x g) and stored in portion aliquot at -80° for further determination of leptin, and tri-iodothyronine.
Body composition was measured in hamsters of experiments A and B by dissection and weighing of the main organs (heart, liver, kidney, stomach, intestine, lungs and spleen) and of the regional adipose depots (white mesenteric, epididymal, retroperitoneal, subcutaneous and brown interscapular).
Tissue removal.
A piece of liver (1 g) and the whole red Vastus lateralis muscle (100–150 mg) of the hamsters of experiment A were used immediately for tissue fractionation in appropriate buffers as described previously (35
), and using conventional ultracentrifugation techniques. The mitochondrial fraction obtained was then stored at -80°C for further determination of carnitine palmitoyltransferase I (CPT-I) activity.
CPT-I activity assay in liver and red Vastus lateralis.
The CPT activity was determined according to the method of Bieber et al. (35
,36
). The results were expressed in specific activity [nmol/(min · mg of protein)] and in tissue capacity [nmol(min · g of wet tissue)]. Protein content was determined according to the method of Lowry (37
).
In vivo NMR determination of body composition.
Proton NMR spectra were recorded at 200 MHz on a Bruker Biospec Avance imaging spectrometer equipped with a 4.7 tesla Bruker magnet BMT 47/30 (Bruker Medical GmbH, Ettlingen, Germany).
Hamsters were lightly anesthetized with Zoletil and set in the NMR probe in a manner similar to a naturally sleeping hamster because this position gave the best spectrum resolution on the whole animal. Hamster position in the center of the magnet was monitored by a rapid imaging method. No respiratory gating was used given the short acquisition time of a single shot spectrum.
The two NMR lines (water and lipids) appearing on the spectrum were integrated with the integration routine of the Bruker WinNMR program. The relative triglyceride content, thus, determined was correlated with the dissection values of adipose tissues obtained by weighing (r = 0.743; P < 0.0001), which agrees well with the other studies using NMR to determine body fatness (38
,39
).
Determination of the incorporation of dietary nitrogen to muscle and liver tissues by isotopic ratio mass spectrometry.
A 1-g portion of liver and thigh muscle was dissected immediately after killing and dried for 15 d at 80°C in a stove. Total N and 15N enrichment in the tissues were then determined using isotope-ratio mass-spectrometry (Optima, Fisons Instruments, Manchester, UK) coupled to an elemental analyzer (NA 1500, Serie 2; Fisons Instruments) as previously described (40
).
Hormonal and glycemic status.
Glycemia was measured on whole blood using a glucometer (Glucometer encore R; Bayer Corporation, Elkhart, IN). Plasma levels of insulin, leptin, and tri-iodothyronine were determined by radio-immuno assay (sensitive rat insulin RIA kit; Linco St. Charles, MO; Leptin multispecies RIA kit; Linco), and T3 kit (Cis Bio-International, Gif sur Yvette, France). The adequacy to the hamster species was tested before the experimental assays. The homeostatic model assessment (HOMA) for insulin resistance was calculated from the insulin and glucose values using the formula: HOMA = insulin (pmol/L)/(9 * 22.5-ln glucose (mmol/L)) (41
).
Statistics.
Results are presented as means ± SEM. Comparisons were made using one-way ANOVA or two-way ANOVA followed by a Student Newman-Keuls post-hoc test. Differences in the relative whole-body triacylglycerol content at two time-points were tested with a paired t test. Indirect calorimetry data were tested using a repeated measures ANOVA with a Scheffé post-hoc (SAS system). 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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Food intake and body weight gain did not differ among the three groups (data not shown).
Components of energy expenditure in free living conditions.
BgM, Gox, Lox and the Lox ratio were recorded for 10 h after the ingestion of the meal (Fig. 1
) and the BM did not differ among the three groups.
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The R group tended to expend less energy with activity than the C (P = 0.054) and the CLA mix (P = 0.15) groups. Although Gox did not differ among the groups, Lox was lower in the R group, in particular late after the meal was ingested (Lox = 16.3 ± 1.8 kJ, in the Control group, 8.9 ± 1.7 kJ in the R group, and 15.7 ± 3.3 kJ in the CLA mix group, respectively, 9 h after the meal, P < 0.05).
Exercise-induced substrate oxidation.
Energy expenditure during exercise on the treadmill was typical of what is generally observed in running rodents (Fig. 2
) (42
).
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CPT-I specific activity in liver and red muscle.
The specific activity of CPT-I, the rate-limiting enzyme in fatty acid oxidation, was significantly higher in both the R- and CLA mix-fed hamsters than in the controls. The activity was greater only in the CLA mix-fed group when expressed as tissue capacity (Table 2
).
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White adipose tissue as well as carcass (defined as bones plus muscles) weights did not differ among groups (data not shown) after 6 or 8 wk of treatment. Relative interscapular brown adipose tissue weight was greater in both CLA groups (P < 0.05) after 6 wk (0.24 ± 0.02 and 0.23 ± 0.02 g/100 g body in the R and CLA mix groups, respectively, and 0.19 ± 0.02 g/100 g in the Control group).
At d 45, the overall relative body triglyceride content measured by NMR was greater in the R group than in the C and CLA mix groups (P = 0.05; Table 3
). The whole-body triglyceride load increased from d 21 to d 45 in the C and the R groups but not in the CLA mix-fed hamsters.
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Irrespective of dietary treatments, the 15N enrichments of liver proteins were greater than in skeletal muscle (Table 4
) (P < 0.0001). Dietary 15N incorporation rate into body proteins was not affected by CLA.
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The basal concentrations of leptin, triiodothyronine and insulin measured on plasma sampled after 18 h of food deprivation did not differ among the groups (Table 5
) although the plasma insulin concentration tended to be greater in the hamsters fed the CLA mix than in controls (P = 0.0543). The blood glucose concentration in the CLA mix-fed group was greater than in both the C and R groups (P < 0.05). The HOMA for insulin resistance was greater in the CLA mix group than in the C and R groups, which did not differ from one another (P < 0.05).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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,22
) and/or lipid oxidation in one or several of the metabolic components of daily energy expenditure. Another possibility is that they reduce both fatty acid uptake and the lipogenic activity of adipose tissue, thereby decreasing adiposity simply by reducing the lipid accumulation/lipolysis ratio over time (23
). To understand which component of energy expenditure is modified by a CLA treatment, we measured energy metabolism and substrate oxidation in hamsters fed diets augmented with a CLA mixture composed with the 9c,11t-isomer and the 10t,12c-isomer or with the 9c,11t-isomer (rumenic acid) alone. Four different physiological conditions where examined: the basal state, the postprandial period, during spontaneous activity and during imposed physical exercise on a treadmill. In addition, the whole-body triacylglycerol content was monitored at 3 and 6 wk to determine whether CLA would induce fat loss with long-term supplementation. The main observation of this study was that after 4 to 5 wk of treatment with CLA, none of the components of energy expenditure was modified by CLA feeding. In contrast, only hamsters fed with the CLA mixture did not gain whole-body triglyceride between d 21 and d 45 of the study. Basal metabolism measured in the postabsorptive state during the 4 h before the test meal indicated that CLA feeding, whether as a mixture (9c, 11t- and 10t,12c-isomers) or as the 9c, 11t-isomer alone, did not affect basal energy expenditure in Syrian hamsters, and that the thermic effect of food was not modified by the CLA-augmented diets compared with the standard diet.
The effect of the feeding state on the energy cost of spontaneous activity was also measured from meal offset until 12 h after feeding. We focused on this specific variable to test the hypothesis that CLA promote body fat loss by favoring lipid oxidation during spontaneous activity in the fed state and/or in the postabsorptive state. The hamsters in the R group generally oxidized less lipid during active periods compared with CLA mix and C groups (P = 0.05 after 9 h). This would explain the small but significantly greater whole-body triglyceride content in the R group at d 45 compared with the other groups, as determined by NMR (Table 3)
. Taken together these data indicate that CLA feeding, especially as a mixture (9c,11t- and 10t,12c-), did not widely affect the various components of energy expenditure. Overall, the various components of energy expenditure (basal, activity-related, or feeding-related) were not affected by diet in freely moving hamsters.
Treadmill exercise was imposed to test the possibility that CLA may favor lipid oxidation by muscles when the workload was greater than during spontaneous activity, and, thus, to test whether regular exercise would improve the efficiency of CLA treatments. The choice of a run at 65% of the maximum aerobic power (VO2max), i.e., at a mild intensity, allowed the untrained hamsters to respond during 2 h to the energy demands of the run, and favored the maintenance of aerobic oxidative processes to fuel the muscular efforts, thus favoring an equilibrium (cross over) in which glucose and lipid oxidation would each account for 50% of energy expenditure (34
) (Fig. 2)
. All the hamsters responded to the beginning of the exercise with a sharp increase in Gox, a response that fits with the classical profile of substrate mobilization in response to exercise and that occurs because glucose is a more readily available substrate than lipid. Then, as the exercise continued, a progressive increase in Lox developed at the expense of Gox. During the 2nd h of exercise, lipids became the major substrate used. During the recovery period, Lox accounted for up to 75% of EE in all groups while it was only 50% of EE before exercise. Thus, Lox was favored not only during the exercise period, but also during the recovery period. The profiles of Gox and Lox during this study were similar in all groups, showing that in Syrian hamsters, CLA feeding does not induce any specific increase in lipid oxidation by the working muscle or during recovery from exercise.
The lack of metabolic adaptations after CLA supplementation are in accordance with the data collected on body composition determined postmortem by tissue weighing, or body fatness determined in vivo using NMR. Both methods clearly indicated that CLA feeding did not affect body composition. However, others have found that feeding Syrian hamsters CLA containing the 10t, 12c-isomer in amounts comparable with our study lowered the fat depots (43
,44
). The several strains of Syrian hamsters appear to respond differently to dietary challenges (45
–47
). It is possible that our strain of hamster is not as responsive to CLA feeding as other strains of Syrian hamsters, as it is the case for the different strains of Zucker rats (48
), and that the genetic polymorphism would greatly modulate the biological effect of CLA. This could be part of the explanation for the discrepancies in fat reduction in people fed CLA (16
,25
). Nevertheless, this result confirms that hamsters are usually less responsive to CLA treatment than mice (10
,17
,26
). However, the triacylglycerol content expressed relative to water did not increase in the CLA mix group between d 21 and d 45 as it did in the R and C groups. This is consistent with the hypothesis of Pariza et al. (23
) in which CLA would block body fat gain, but not necessarily reduce body fat level which had accumulated before CLA administration. This would also explain the lack of large modifications in energy metabolism in hamsters fed CLA. The determination of whole-body triacylglycerol content by NMR measures extra adipose tissue triacylglycerol. This would explain why a CLA effect on body fat was shown in one case (NMR determination), whereas it was not in the other (tissue dissection). In addition, the body water content varies inversely to that of body fat, which makes the NMR determination based on the triacylglycerol/water ratio more accurate than weighing adipose tissue.
Tri-iodothyronine and leptin are both expected to increase with resting energy expenditure. The CLA diets did not affect the basal plasma concentrations of these hormones, consistent with the lack of effects on the various components of energy expenditure. Moreover, similar leptin levels are consistent with the adiposity assessed by weighing white adipose tissues.
The higher CPT-I-specific activities in the liver and red muscle tissues of the CLA-fed hamsters did not correlate with an increased rate of lipid oxidation at rest in response to feeding or during exercise. This effect seems paradoxical because the in vitro CPT-I activity is usually associated with the in vivo rate of fatty acid oxidation (49
,50
). One possible explanation may be a down-regulation of lipid oxidation at the CPT-I level through an increased sensitivity to malonyl-CoA in the CLA-fed groups. Also, the high concentrations of insulin and glucose in the CLA mix group would counteract to some extent the potentially greater channeling of fatty acids toward oxidation through the CPT-I system. The comparable use of lipids to fuel exercise despite higher CPT-I activities in active muscle of the CLA groups (Vastus lateralis is part of the quadriceps femoris complex) during the run suggests a reduced substrate availability, i.e., fewer free fatty acids arising from the adipose stores (mobilization or transport into myocytes), or greater regulation at the level of CPT-I by the higher cellular malonyl-CoA.
The 15N enrichment into muscle and liver from 15N-labeled dietary casein was used as an index of protein synthesis and was observed by others to be increased by CLA-augmented diets in growing mice (10
). This method seemed sufficiently sensitive to detect differences in protein turnover because, on average, the excess 15N enrichment in livers was 4.57 higher than in muscles (P < 0.0001), consistent with the higher metabolic activity and protein turnover in this tissue (51
), (52
). In contrast, the dietary treatments did not affect the 15N enrichments. This result appears consistent with the fact that no differences were reported for muscle mass measured after 8 wk of treatment by weighing the carcasses. However, it is possible that the procedure used here was not sensitive enough to detect small changes in metabolism and protein synthesis rate.
Contrary to the control group and to the 9c,11t-isomer fed group, the hamsters fed the CLA mix did not accumulate fat during the study. Nevertheless, our strain of hamsters appears to be poorly responsive to CLA treatment with regard to body protein accumulation and fat reduction and any of the components of energy expenditure. Comparative studies carried out with comparable dietary conditions with clearly identified CLA isomers are required to understand why in some species, e.g., mice, CLA treatment efficiently reduces body fatness (20
,43
,53
–56
), whereas in other species (or even among different strains of the same species), it is much less effective (this study) (24
,25
,56
) and what would be the physiological conditions that support the best potential for CLA to be efficacious.
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FOOTNOTES |
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Manuscript received 8 January 2002. Initial review completed 20 February 2002. Revision accepted 19 June 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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