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The Journal of Nutrition Vol. 129 No. 1 January 1999,
pp. 92-97
Department of Animal Science, Texas A&M University, College Station, TX 77843-2471
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ABSTRACT |
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Abstract
Introduction
Methods
Results
Discussion
References
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This study documented the effects of conjugated linoleic acid (CLA) on the proliferation and differentiation of 3T3-L1 preadipocytes. During proliferation, preadipocytes were cultured in Dulbecco's modified Eagle's medium (DMEM), 100 g/L fetal bovine serum (FBS), 0.584 g/L L-glutamine and 0 (control), 0.5, 1.0, 5.0 or 10.0 mg/L CLA. Proliferation of 3T3-L1 preadipocytes was measured directly by cell counting and indirectly by radiolabeled thymidine incorporation into DNA at 96 h postinoculation. Conjugated linoleic acid was not cytotoxic during proliferation or differentiation. The 0.5, 1.0, 5.0 or 10.0 mg/L CLA treatments inhibited proliferation by 8, 12, 31 and 36%, respectively (all P < 0.05). Treatment with 10 mg/L CLA or 10 mg/L linoleic acid (cis-9,12) reduced the incorporation of 3H-thymidine into DNA by 56 and 35%, respectively, suggesting that some portion of the effect of CLA on preadipocyte proliferation was nonspecific. After the initiation of differentiation, preadipocytes were cultured in DMEM, 100 g/L FBS, 0.584 g/L L-glutamine, 1.7 µmol/L insulin and 0 (control), 0.5, 1.0, 5.0 or 10.0 mg/L CLA. Radiolabeled glucose incorporation into cellular lipids was increased from 7.4 to 11.1, 11.1, 17.4 and 22.5 nmol/(h·106 cells) (all P < 0.05) by 0.5, 1.0, 5.0 and 10.0 mg/L CLA, respectively. A media concentration of 10 mg/L CLA increased total cellular CLA (from 0 to 0.16 ± 0.01 µmol/106 cells), palmitic acid (from 0.47 to 1.10 ± 0.03 µmol/106 cells) and palmitoleic acid (from 0.24 to 0.81 ± 0.03 µmol/106 cells) (means ± pooled SEM; all P < 0.05). Conjugated linoleic acid had no effect on arachidonic acid content, but decreased its proportion (g arachidonic acid/100 g total fatty acids) by >50% (P < 0.05). These data indicate that CLA inhibited proliferation and promoted de novo lipogenesis and lipid filling in 3T3-L1 preadipocytes, suggesting that CLA may reduce overall fat accumulation in growing animals by inhibiting stromal vascular preadipocyte hyperplasia.
KEY WORDS: CLA · proliferation · differentiation · mice · preadipocyte · obesity
Conjugated linoleic acid (CLA)5 is the collective acronym for combinations of positional and geometric isomers of linoleic acid that exist naturally in dairy products and meats. It is produced in ruminant animals via biohydrogenation of polyunsaturated fatty acids as well as during the mechanical processing of dairy products (Chin et al. 1992 Conjugated linoleic acid recently was reported as a potent regulator of body fat accumulation and retention. Pariza et al. (1996) The purpose of this study was to examine further the potential of CLA to regulate body fat accumulation and retention, possibly via modulation of adipocyte hypertrophy and/or preadipocyte hyperplasia. It specifically explored the effects of CLA on 3T3-L1 preadipocyte proliferation and differentiation in culture.
Culture conditions.
Murine 3T3-L1 preadipocytes were cultured in growth media consisting of Dulbecco's modified Eagle's medium (DMEM), 100 g/L fetal bovine serum (FBS) and 0.584 g/L L-glutamine. The cells were incubated at 37°C in a humidified, 5% CO2 atmosphere. Conjugated linoleic acid was obtained from Nu-Chek-Prep (Elysian, MN) and consisted of 41% cis-9, trans-11/trans-9, cis-11, 44% trans-10, cis-12, and 10% cis-10, cis-12 isomers. Other CLA isomers comprised ~5%, and cis-9,12 linoleic acid comprised <1% of the total. Conjugated linoleic acid was diluted in ethanol and administered at concentrations of 0 (control), 0.18, 0.36, 1.78 and 3.57 × 10 Trypan blue exclusion.
Samples were diluted (1:1) with 0.5 mL of 4 g/L trypan blue in 8.5 g/L saline solution. The number of viable and nonviable cells was counted with a hemocytometer.
Lactate dehydrogenase activity.
At 96 h postinoculation (72 h post-CLA administration) for proliferation, and at 6 d postinduction of differentiation, lactate dehydrogenase activity of the media was measured as the reduction of pyruvic acid at 340 nm with a Beckman model DU-7 spectrophotometer (Beckman Instruments, Palo Alto, CA). Lactate dehydrogenase activity was expressed as µmol NADH consumed/(min·L medium).
Radiolabeled thymidine incorporation into DNA.
Incorporation of 3H-thymidine into 3T3-L1 preadipocyte DNA was determined using the trichloroacetic acid precipitation method described by Koohmaraie (1987) Cell number.
At 96 h postinoculation, aliquots of each sample were diluted (1:1) with 0.5 mL of 4 g/L trypan blue in 8.5 g/L saline solution. The number of cells was counted with a hemocytometer.
Oil Red O staining.
At 6 d postinduction of differentiation, the cells were fixed by 24-h incubation in 100 g/L formalin solution and stained with Oil Red O solution for 1 h. The nuclei were counterstained with Mayer's hematoxylin (1 g/L) for 3 min (Strutt et al. 1996 Glucose incorporation into lipids.
Cells were incubated for 2 h with 18.3 MBq [U-14C]glucose/L 6 d after the first addition of CLA and differentiation-inducing medium. Lipids were extracted as described (May et al. 1994 Analysis of cellular lipids.
Differentiated cells were prepared for gas chromatography analysis by extraction, saponification and methylation of cellular lipid. Total lipids were extracted by the Folch procedure (Folch et al. 1957), and the extracted lipids were methylated according to the procedure of Morrison and Smith (1964) Analysis of data.
One-way ANOVA was performed to determine significance of differences. Means were separated by Fisher's Least Significant Difference method and differences were considered significant at P < 0.05.
Source of chemicals.
Unless otherwise stated, biochemicals were purchased from Sigma Chemical (St. Louis, MO) and Gibco BRL (Gaithersburg, MD). Radiolabeled materials were obtained from Amersham (Arlington Heights, IL).
The effect of conjugated linoleic acid on 3T3-L1 preadipocyte viability.
The addition of CLA to the culture medium did not affect (P < 0.05) the ability of cells to exclude trypan blue at 96 h postinoculation, or at 6 d postdifferentiation. A 100% cellular lysis occurred in response to administration of 100 mg/L CLA for 24 h. Lactate dehydrogenase activities in the cell media at 96 h during proliferation and at 6 d postinduction of differentiation were not different (P > 0.05) among treatments (data not shown). Lactate dehydrogenase activity in the media was reduced from 22 µmol/(min·L) in control cultures to 19 µmol/(min·L) in cultures containing 0.5 or 1 mg/L CLA at 6 d postinduction of differentiation. There also was an increase in activity to 25 µmol/(min·L) in cells cultured with 10 mg/L CLA. These values were marginally different from control (P = 0.06). The low overall lactate dehydrogenase activity, coupled with a lack of significant difference among treatment groups, indicated that CLA was not cytotoxic to proliferating or differentiating 3T3-L1 cells at concentrations as high as 10 mg/L. These results were consistent with those reported in human MCF-7 breast cancer cells by Cunningham et al. (1997) The effect of CLA on 3T3-L1 preadipocyte proliferation.
There was a 7.2-fold increase in cell number from inoculation to 96 h for control preadipocytes (data not shown). There were overall decreases of 7.7, 11.5, 31.2 and 35.8% in cell number (P < 0.05) compared with control for 0.5, 1, 5 and 10 mg/L CLA, respectively (Fig. 1).
The effects of CLA on 3T3-L1 preadipocyte differentiation.
Treatment of 3T3-L1 cells with increasing CLA concentrations in differentiation-inducing media caused increases of 32.7, 33.1, 57.4 and 67.0% (P < 0.05) in glucose incorporation into the neutral lipids of 3T3-L1 cells (Fig. 4). Similarly, a progressive increase in cellular lipid content from control through 1, 5 and 10 mg/L CLA was visibly evident in 3T3-L1 cells stained with Oil Red O (Fig. 5).
This study documented the effects of CLA on 3T3-L1 preadipocyte proliferation and differentiation. Several investigators have reported that CLA is an effective regulator of body fat accumulation and retention (Belury and Kempa-Steczko 1997
INTRODUCTION
Abstract
Introduction
Methods
Results
Discussion
References
, Gurr 1987, Kepler and Tove 1967, Viviani 1970). The cis-9, trans-11 isomer is particularly enriched in the phospholipid fraction of rat cell membranes (Ha et al. 1989, Huang et al. 1994, Kramer et al. 1998, Sebedio 1997). Conjugated linoleic acid is incorporated into hepatic phospholipids at the expense of linoleic acid (Belury and Kempa-Steczko 1997). Conjugated linoleic acid has proven to be anticarcinogenic and antitumorogenic (Belury et al. 1993 and 1996, Cesano et al. 1998, Cunningham et al. 1997, Ha et al. 1990, Ip et al. 1991, Ip 1997, Schultz et al. 1992). The anticarcinogenic effect of CLA originally was proposed to be mediated by its antioxidative properties (Chin et al. 1993, Ha et al. 1990, Ip et al. 1991, Pariza et al. 1991). More recently, evidence indicates that CLA reduces tumorogenesis by depressing prostaglandin E2 synthesis (Belury and Kempa-Steczko 1997, Liu and Belury 1998).
reported that mice, rats and chicks fed diets containing 0.5% CLA plus 5.0% corn oil for 4-8 wk experienced body fat reductions of 57-70, 23 and 22%, respectively. Belury and Kempa-Steczko (1997) reported significantly lower body weights in rats as a result of 1.0 and 1.5% dietary CLA supplementation for 6 wk.
MATERIALS AND METHODS
Abstract
Introduction
Methods
Results
Discussion
References
5 mol/L, corresponding to 0, 0.5, 1, 5 and 10 mg/L, respectively. Final ethanol concentration in the growth medium was 0.1%. In additional studies, some flasks received 10 mg/L linoleic acid. Conjugated linoleic acid or linoleic acid was added 24 h postinoculation to allow adherence of the cells to the flask substratum.
, Student et al. 1980).
. At 72 h postinoculation (48 h post-CLA administration), cells were incubated for 24 h with 9.17 MBq [3-3H]thymidine/L medium. The incorporation of 3H-thymidine was determined by liquid scintillation counting (Model LS3800, Beckman Instruments) and expressed as Bq/106 cells. Cell counts were determined from parallel treatment groups at the time of radiolabeled thymidine measurement.
).
). The incorporation of 14C-labeled glucose into neutral lipids was determined by liquid scintillation counting and expressed as nmol glucose/(h·106 cells). Cell counts were determined from parallel treatment groups at the time of radioisotope addition to the medium.
, modified to include four times the prescribed amount of boron trifluoride. Fatty acid methyl esters were extracted into hexane and analyzed on a Packard Chrompack (Packard Model 437 A, Chrompack, Raritan, NJ) gas chromatograph. Fatty acid methyl esters were separated on a 2 m × 2 mm (i.d.) column packed with 15% CP-Sil; nitrogen was the carrier gas. Detector and injector temperatures were 250°C; the column was run isothermally at 160°C until stearic acid methyl ester eluted (~8 min), after which the temperature was increased 10°C/min to 220°C. Methyl laurate (5 mg) was added to each sample to serve as the internal standard. Fatty acid peaks were identified by comparison to an external standard (Nu-Chek-Prep). Under these conditions, the CLA-methyl esters eluted as a single peak. The retention time and identity of this peak were verified by methylating and analyzing 5 mg of the CLA preparation used for the preadipocyte cultures. Areas of the peaks were quantified with a Spectraphysics SP4290 recording integrator (Spectraphysics, San Jose, CA). Quantification of fatty acids was calculated by ratio analysis of sample area under peak to the area of the methyl laurate internal standard. Concentrations also are expressed gravimetrically.
RESULTS
Abstract
Introduction
Methods
Results
Discussion
References
and Schultz et al. (1992).
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Fig 1.
Total cell number per 25 cm2 flask and tritiated thymidine incorporation into DNA in murine 3T3-L1 preadipocytes treated with conjugated linoleic acid during proliferation. The number of cells was measured 96 h postinoculation with a hemocytometer. At 72 h postinoculation, the cells were incubated for 24 h in the presence of [3-3H]thymidine. Tritiated thymidine incorporation (3H incorporation) was measured by liquid scintillation counting and expressed as Bq/106 cells. Cell number was obtained from parallel treated flasks counted with a hemocytometer at the time of radiolabeled thymidine incorporation measurement. Values are means ± pooled SEM, n = 5. *Different from control (P < 0.05). **Different from control (P < 0.001) and different from treatment with 0.5 mg/L linoleic acid (P < 0.05).
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Fig 2.
Proliferation of murine 3T3-L1 preadipocytes cultured in the absence or presence of conjugated linoleic acid. Micrographs were taken at 5, 24, 48, 72 and 96 h postinoculation, for control (a-e) or treatment with 10 mg/L conjugated linoleic acid (CLA) (f-j). Scale bar is indicated in (a).
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Fig 3.
Tritiated thymidine incorporation into DNA and media lactate dehydrogenase activity in control murine 3T3-L1 preadipocytes and preadipocytes treated with 10 mg/L conjugated linoleic acid or 10 mg/L linoleic acid during proliferation. At 72 h postinoculation, the cells were incubated for 24 h in the presence of [3-3H]thymidine. Tritiated thymidine incorporation was measured by liquid scintillation counting and expressed as Bq/106 cells (3H incorporation). Samples of media were analyzed for lactate dehydrogenase activity at 96 h postinoculation. Values are means ± pooled SEM, n = 4. *Different from control (P < 0.05). **Different from control (P < 0.001) and different from treatment with 10 mg/L linoleic acid (P < 0.05).
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Fig 4.
Glucose incorporation into cellular lipid during differentiation in murine 3T3-L1 preadipocytes treated with conjugated linoleic acid. At 6 d postinduction of differentiation, cells were incubated for 2 h in the presence of [U-14C]glucose. Radiolabeled glucose incorporation into lipid was measured by liquid scintillation counting and expressed as nmol glucose/(h·106 cells). Cell number was obtained from parallel treated flasks and counted using a hemocytometer at the time of addition of radiolabeled glucose. Values are means ± pooled SEM, n = 4. *Different from control (P < 0.05). **Different from control (P < 0.01) and different from treatment with 0.5 or 1 mg/L conjugated linoleic acid (P < 0.05).
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Fig 5.
Lipid filling of murine 3T3-L1 preadipocytes cultured in the absence or presence of conjugated linoleic acid. Preadipocytes were incubated with (a) 0, (b) 1 mg/L, (c) 5 mg/L or (d) 10 mg/L conjugated linoleic acid (CLA) for 6 d after initiation of differentiation protocol. Cellular lipid was stained with Oil Red O. Cell nuclei were counterstained with Mayer's hematoxylin solution. Scale bar is indicated in (a).
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Fig 6.
Contents (µmol/106 cells; a) and proportions (g/100 g total fatty acids; b) of cellular fatty acids in murine 3T3-L1 cells treated with 0 (control), 5 or 10 mg/L conjugated linoleic acid (CLA) during differentiation. At 6 d postinduction of differentiation, samples were prepared for gas chromatographic analysis by extraction, saponification and methylation of cellular lipids. The fatty acid methyl esters were analyzed by gas chromatography. Cell number was obtained from parallel treated cells and counted using a hemacytometer. Values are means ± pooled SEM, n = 3. *Different from control (P < 0.05). **Different from treatment with 0 (control) or 5 mg/L conjugated linoleic acid (P < 0.05).
DISCUSSION
Abstract
Introduction
Methods
Results
Discussion
References
, Pariza et al. 1996, Park et al. 1997, Sisk et al. 1998). Sisk et al. (1998) demonstrated that CLA reduced adipocyte volume in Sprague-Dawley rats sufficiently to account for the reduction in adipose tissue mass. Our data suggest that CLA could depress body fat accumulation by reducing preadipocyte number if provided during periods of hyperplastic growth.
, who demonstrated that 104 mol/L CLA (~28 mg/L) reduced lipoprotein lipase activity and increased lipolysis in 3T3-L1 preadipocytes. Had the same occurred in our experiments, it is unlikely that we would have observed increased adipocyte size and lipid content in response to treatment of preadipocytes with CLA.
may have been due to the higher concentration of CLA used in the earlier investigation. We did not establish the maximum concentration of CLA to which preadipocytes could be exposed, but treatment of cells with 100 mg/L CLA was completely toxic. The stimulation of de novo lipogenesis by CLA, in conjunction with the maintenance of cell viability (trypan blue exclusion and low media lactate dehydrogenase activity), indicated strongly that CLA was not cytotoxic at concentrations up to 10 mg/L.
), CLA was incorporated into the total lipid fraction of differentiating 3T3-L1 cell in a dose-dependent manner. The large increase in 16-carbon fatty acids (palmitic and palmitoleic) suggests a stimulation of acetyl CoA carboxylase and/or fatty acid synthetase activity by CLA (consistent with the greater incorporation of radiolabeled glucose into total lipids). Conversely, the lesser increases in stearic and oleic acids indicated that fatty acid elongase activity was not stimulated by CLA, leading to a limitation in the rate of synthesis of 18-carbon fatty acids. Increases in palmitoleic and oleic acid elicited by CLA were substantially greater than those observed for palmitic or stearic acid, suggesting that stearoyl-CoA desaturase gene expression was stimulated by CLA administration.
reported that prostaglandin F2
strongly inhibited 3T3-L1 preadipocyte differentiation. This was accompanied by a complete inhibition of stearoyl-CoA desaturase gene expression (Ntambi 1998). Because CLA elicited essentially opposite effects, the data suggest that CLA may have worked by inhibiting prostaglandin F2 synthesis. Conjugated linoleic acid is incorporated into hepatic phospholipids at the expense of linoleic acid in mice fed CLA (Belury and Kempa-Steczko 1997), which would reduce substrate availability for prostaglandin synthesis. In this investigation, the percentage of arachidonic acid in total cellular lipids was reduced by >50%. This is similar to effects observed in hepatic neutral lipids of mice (Belury and Kempa-Steczko 1997) and phospholipids of keratinocytes (Liu and Belury 1998) treated with CLA. The data therefore suggest that the stimulation of fatty acid synthesis and accumulation (and possibly desaturation) we observed in preadipocytes treated with CLA during differentiation may have been caused by a reduction in prostaglandin synthesis.
. C/EBP is not expressed during proliferation in 3T3-L1 preadipocytes (Umek et al. 1990) but is highly induced by the onset of differentiation in 3T3-L1 preadipocytes (Christy et al. 1991). It has been proposed that C/EBP functions to terminate mitotic clonal expansion that occurs early in differentiation in addition to being required to induce adipocyte differentiation (Mandrup and Lane 1997). Our results are consistent with a stimulation of C/EBP gene expression by CLA treatment of 3T3-L1 preadipocytes.
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FOOTNOTES |
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Manuscript received 4 May 1998. Initial reviews completed 25 June 1998. Revision accepted 30 October 1998.
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LITERATURE CITED |
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Abstract
Introduction
Methods
Results
Discussion
References
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is a potent inhibitor of 3T3-L1 preadipocyte differentiation. FASEB J. 12: A515 (abs.).This article has been cited by other articles:
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