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ANIMAL GROWTH, PHYSIOLOGY, AND REPRODUCTION |
Department of Animal Science, National Taiwan University, Taipei 106, Taiwan
Abstract
To study the effect of dietary docosahexaenoic acid (DHA) on the expression of adipocyte determination and differentiation-dependent factor 1 (ADD1) mRNA in pig tissues, weaned, crossbred pigs (30 d of age) were fed either 2% (as-fed basis) tallow or DHA oil for 18 d. Body weight of the pigs was not affected by different dietary fatty acid (FA) compositions. The plasma and liver FA composition reflected the composition of the diet. The adipose tissue and skeletal muscle FA composition only partially reflected the diet, indicating either a slower FA turnover or that a greater proportion of the FA in these tissues is from endogenous FA synthesis. The ADD1 is an important transcription factor that modulates transcription of FA synthase to regulate the endogenous FA synthesis in the liver and adipose tissue. The ADD1 mRNA was decreased (P < 0.05) in the liver of DHA-treated pigs compared with that of the tallow-treated pigs. The diets did not have an effect on the ADD1 mRNA in pig adipose tissue. The ADD1 transcript was not detected in pig skeletal muscle. These results indicate that significant enrichment of liver DHA content inhibits the expression of ADD1 mRNA. Such an effect is similar to that reported in porcine differentiating adipocytes cultured with DHA. The liver and muscle acyl CoA oxidase mRNA concentration was increased (P < 0.05) by DHA oil treatment, suggesting that DHA treatment may increase peroxisomal fatty acid oxidation in these two tissues. Our present observations demonstrate that dietary DHA enrichment not only affects tissue DHA concentration but also mildly modifies the expression of genes related to fatty acid metabolism in the porcine liver and skeletal muscle.
Key Words: Acyl-CoA Oxidase • Adipocyte Determination and Differentiation-Dependent Factor 1 • Docosahexaenoic Acid • Fatty Acid Synthase • Pigs
Introduction
Individual long-chain fatty acids (FA) stimulate differentiation of clonal preadipocytes (Amri et al., 1991
: Distel et al., 1992). Several long-chain FA (stearic acid, oleic acid, and arachidonic acid) also stimulate porcine preadipocyte differentiation in a cell culture system (Ding and Mersmann, 2001; Ding et al., 2002, 2003b). However, incubation of porcine preadipocytes with docosahexaenoic acid (DHA; C22:6) had no effect on adipocyte differentiation (Ding et al., 2002). Individual FA have different effects on adipocyte physiology.
The transcription factor, adipocyte determination and differentiation-dependent factor 1 (ADD1), also called sterol regulatory element-binding protein 1c, regulates the transcription of fatty acid synthase (FAS) and plays a role in adipocyte differentiation (Kim and Spiegelman, 1996; Kim et al., 1998). The ADD1 messenger RNA (mRNA) is highly transcribed in both porcine adipose tissue and liver (Ding et al., 1999, 2000). Dietary fish oils decrease hepatic FAS through a reduction of ADD1 expression in rodents (Xu et al., 2001). Incubation of porcine preadipocytes in vitro (i.e., stromal-vascular cells) with DHA decreased ADD1 mRNA and protein concentrations (Ding et al., 2002; Hsu and Ding, 2003). The DHA may suppress expression of ADD1 that in turn decreases fatty acid biosynthesis. However, dietary fish oil (mixture of FA) has minimal effects on the abundance of transcripts in porcine adipose tissue and liver (Ding et al., 2003a), indicating the effect of FA on porcine gene expression in vivo may be different from that of rodents. In the current study, high-DHA algal oil was added to the diet for pigs to test the hypothesis that dietary DHA has the effect of inhibiting ADD1 mRNA in both adipose tissue and liver. Transcripts for other genes associated with FA metabolism also were measured in adipose tissue, liver, and skeletal muscle.
Materials and Methods
Animals and Diets
The animal protocol used in the present experiment was approved by the Animal Care and Use Committee of the Animal Technology Institution in Taiwan. Weaned, crossbred pigs (21 d of age) were purchased from a commercial pig farm and transported to the Animal Technology Institute in Taiwan. They weighed 5.3 ± 0.6 kg and were fed the control diet (Table 1) for 9 d to help them to acclimate to the diet and the environment. At 30 d of age, the pigs were fed a diet supplemented with either 2% (as-fed basis) tallow or an algal DHA containing oil for 18 d (12 pigs per group). The 2% DHA oil supplementation was chosen because such supplementation should enrich the dietary DHA to a level similar to that of 10% dietary fish oil addition. The calculated protein content in the experimental diets was 23%, and the calculated fat was 4.62% on an as-fed basis for the diets. The FA composition of the diets was analyzed and is indicated in Table 2. Beginning 3 d before administration of the experimental diets, pigs were fed two meals per day, one at 0700 and the other at 1600. The pigs were fed to approximate ad libitum feeding, with the amount of feed provided reflecting the feed intake of previous day. Pigs from each of the four treatments were housed in a group.
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Fatty Acid Analysis
The FA analysis procedure was a modification of Ding et al. (2003a). In short, a tissue sample was homogenized and then extracted with chloroform and methanol. Before the extraction was begun, 1,000 nmol of heptadecanoic acid (17:0), as di-17:0 L-
-phosphatidylcholine (Sigma, St. Louis, MO) was added to the sample as an internal standard. The extract was subjected to water-bath sonication for 30 min to assist extraction. Samples were centrifuged for 10 min at 3,000 x g, the lower chloroform layer was collected, and the sample was extracted once more with chloroform. The combined chloroform phases were washed with 1.5 mL of methanol:water:chloroform (47:48:3, vol/vol/vol) and then dried at room temperature under nitrogen gas. The total lipid residue from plasma, diet, or tissue homogenates was hydrolyzed and then methylated with HCl/methanol. Hexane and water were used to extract fatty acid methyl esters. The fatty acid methyl esters were separated by gas chromatography on a 60 m x 0.53 mm i.d. Sulpelcowax-10 capillary column (1.00 mm film thickness; Sulpeco Inc., New Territories, Hong Kong), with a Varian Star 3400cx gas chromatograph (Varian Technologies, Wakefield, RI) equipped with a hydrogen flame ionization detector. The temperature gradient for elution of the esters was 120°C at start for 7 min, then ramped at 5°C/min to 250°C (45 min total), and held at 250°C for 5 min before reinitialization. Individual FA were identified by comparison with the retention times of standards (Nu Check Prep, Inc., Elysian, MN). The moles per 100 moles of each FA were calculated from the chromatograms using a proportional comparison of FA peak areas, after each was normalized against the FA molecular mass and flame ionization response factor, to the correspondingly normalized area of the 17:0 internal standard (1,000 nmol, 17:0 per volume of extracted sample). The chromatographic analysis was in duplicate and the data were averaged.
RNA Analysis
Total RNA was extracted from the tissues following the procedure described by McNeel and Mersmann (1999). The RNA was separated by electrophoresis, blotted to membranes, and hybridized with radiolabeled complementary DNA probes in Ultrahyb (Ambion Inc., Austin, TX). The porcine 18S, acyl CoA oxidase (ACO), ADD1, and FAS probe sequences were as previously described (Ding et al., 1999, 2000). The FAS probe was derived from a clone provided by Steven Clarke, University of Texas (Mildner and Clarke, 1991). Hybridization results were quantified by phosphor-image analysis as previously described (Ding et al., 2000; McNeel et al., 2000a). The densitometric value for an individual transcript in a sample lane was normalized to the densitometric value for the 18S ribosomal RNA in the same lane.
Statistical Analysis
Data were analyzed by ANOVA the GLM procedure in SAS (SAS Inst., Inc., Cary, NC) with dietary treatment and feeding status as two major factors. Because the difference of the data from the fed and fasted groups was not significant, the means of pooled data (fed and fasted) were analyzed using a Student’s t-test.
Results
Animal Growth
The DHA contents of the control and treatment diets were 0.25 and 12.69% of the total FA, respectively. Pigs in all feeding groups gained a similar amount of BW over the 18-d period: 4 kg on average (Table 3). The BW of the pigs was not affected by different dietary FA composition.
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Because FA composition for all the tested samples did not show a significant fed or fasted effect, all the FA composition data were pooled data from both sampling times. The DHA contents in the plasma of the tallow- and DHA-fed pigs were 2.37 and 16.43% of total FA (Table 4), respectively, indicating that plasma DHA reflects the dietary DHA enrichment. Plasma C18:0 was reduced (P < 0.05) in the DHA treatment group compared with the control group. Other FA were not affected by the dietary treatments.
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The DHA contents were 0.19 and 1.60% of total FA in the adipose tissue from the tallow- and DHA-fed pigs, respectively, indicating that DHA treatment increases DHA content in the adipose tissue (P < 0.05; Table 5). The incorporation of DHA into adipose tissue only partially reflects the dietary DHA content. The adipose tissue in DHA-treated pigs had more C16:0, C18:0, and C18:1 than that in the tallow-fed pigs. The DHA contents were 0.83 and 2.36% in the skeletal muscle of the tallow- and DHA-fed pigs (P < 0.05; Table 5), respectively, indicating that the DHA treatment significantly increases DHA content in the muscle. The muscle DHA content in DHA-treated pigs was not proportional to dietary DHA content, and muscle deposited more C16:0 and C18:0.
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Because transcript concentrations (Figures 1 to 3) for the genes measured did not show a significant fed or fasted effect, all the data were pooled data from both sampling times. The dietary FA composition did not have an effect on the ADD1 mRNA in pig adipose tissue in either the fed or fasted condition (Figure 1). The ADD1 mRNA was decreased in the liver of DHA-treated pigs compared with the tallow-treated pigs (Figure 1). Both fed and fasted pigs were observed to have about a 35% decrease in hepatic ADD1 mRNA concentration. The result suggests that the great enrichment of liver DHA content (9%) inhibits the expression of ADD1 mRNA. Such an effect is similar to that which was reported in porcine differentiating adipocytes. The ADD1 mRNA was not detectable in pig skeletal muscle (Figure 1), as previously observed (Ding et al., 2000). The FAS mRNA expression in neither adipose tissue nor liver was affected by dietary DHA supplementation (Figure 2). The FAS mRNA was not detectable in pig skeletal muscle. The liver and muscle acyl CoA oxidase mRNA concentration was increased by DHA oil treatment (Figure 3), suggesting that DHA treatment increases peroxisomal FA oxidation in these two tissues. The ACO mRNA in adipose tissue was not affected by different dietary FA composition.
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It has been well documented that dietary FA can be incorporated to a large extent into tissues (Sink et al., 1964; Mason and Sewell, 1967; Eder et al., 2001) and plasma lipids in pigs (Smith et al., 1996; Ding et al., 2003). We have observed changes in tissue FA composition after only 2 wk of feeding a high-fat diet containing 17% fat with 7.2% DHA in the total FA (Ding et al., 2003a). In the current study, with low-fat diets (4.62% total fat by calculation with 12.7% DHA in the total FA), we also observed that dietary DHA enrichment increased tissue DHA. The changes in FA composition in different tissues are very similar to those seen with the high-fat diet experiments (Ding et al., 2003), indicating that the pigs in the current experiment can digest and utilize dietary FA in a fashion similar to that of pigs fed high-fat diets with different FA compositions. These data also show that the weaned piglets digested algal oil and utilized the FA in it, and incorporated DHA to a greater extent into liver than into skeletal muscle or adipose tissue. Differences between diet and tissue FA composition may result from endogenous FA synthesis coupled with elongation of FA chains, desaturation, and specific incorporation of individual FA into complex lipids, as dictated by the selectivity of the enzymes synthesizing the phospholipids, cholesterol esters, and diacylglycerol and triacylglycerol (Lands et al., 1990).
Transcription factor ADD1 is expressed in the liver and adipose tissues in pigs, rodents, and chickens (Ding et al., 1999, 2000; Gondret et al., 2001). It controls the expression of several lipogenic genes (e.g., FAS, acetyl CoA carboxylase, and glycerol-3-phosphate acyltransferase) (Brown and Goldstein, 1997). The expression of rodent hepatic ADD1 is inhibited by dietary fish oil and safflower oil, which contains high concentrations of PUFA (Xu et al., 1999; Yahagi et al., 1999). Previously, we showed that ADD1 mRNA was decreased in differentiating porcine stromal/vascular cells in culture (Ding et al., 2002; Hsu and Ding, 2003). The current study showed the porcine hepatic ADD1 mRNA was significantly reduced by dietary DHA enrichment. The result was similar to that seen with rodents fed fish oil (Xu et al., 1999). Because we observed a considerable decrease in both the ADD1 mRNA and protein in differentiating porcine preadipocytes acutely treated with DHA (Ding et al., 2002; Hsu and Ding, 2003), we expected that there would be a decrease in adipose tissue ADD1 in vivo in pigs fed DHA oil, with an elevated concentration of DHA. However, the adipose tissue ADD1 mRNA was not affected by the dietary DHA treatment. Since the hepatic DHA in the DHA-treated pigs was enriched to more than 9% of total FA, whereas the DHA content in the adipose tissue was just 1.60% of the total FA, we postulate that the inability of dietary DHA enrichment to regulate the expression of ADD1 in porcine adipose tissue results from the relatively low level of DHA deposition. The data also confirmed the results of a previous study indicating that feeding pigs a diet containing a high concentration of fish oil resulted in reduced hepatic ADD1 mRNA but had no effect on ADD1 mRNA in adipose tissue (Ding et al., 2003a). Even though the expression of FAS has been demonstrated to be downregulated by PUFA in rodent liver (Xu et al., 1999) and porcine adipocytes (Hsu and Ding, 2003), the FAS mRNA concentration in porcine liver and adipose tissue was not affected by dietary DHA. The results indicate that in vivo regulation of the expression of FAS is different from that in vitro and that there are species-specific regulatory mechanisms involved in PUFA effects. Because FA synthesis in porcine liver occurs to a lesser extent than in the adipose tissue, the inability of DHA to modify the expression of ADD1 and FAS in adipose tissue suggests that DHA is not very effective in modifying overall FA synthesis in pigs.
The rate-limiting enzyme for peroxisomal FA ß-oxidation is ACO, whose expression is regulated by peroxisome proliferator-activated receptor- (PPAR; Bell et al., 1998; Desvergne and Wahli, 1999). The DHA is one of the candidate ligands for PPAR (Kliewer et al., 1997), therefore activation of PPAR by DHA could increase the expression of ACO. The current experiment showed that DHA accumulated to a great extent in the livers and muscles of DHA-treated pigs, and this was accompanied by elevated abundance of the ACO mRNA. The ACO mRNA in adipose tissue was not affected by the DHA treatment. Similar observations were reported previously in pigs fed fish oil-containing diets (Ding et al., 2003a).
The current experiment also demonstrated that short-term fasting (8 h) feed restriction did not change the mRNA concentrations for ACO, ADD1, or FAS in pig adipose tissue, liver, and skeletal muscle. This observation that short-term energy restriction was not effective in modifying adipose gene expression is similar to that which was reported in the literature (Spurlock et al., 1998; McNeel and Mersmann, 2000; McNeel et al., 2000b). However, we also observed that short-term fasting (8h) blocked the expression of stearoyl coenzyme A desaturase mRNA in porcine subcutaneous fat tissue (our unpublished data), suggesting that the effect of short-term fasting on porcine gene expression is gene specific.
Taken together, these data suggest that a dietary DHA treatment may decrease the expression of genes related to fat synthesis and increase the expression of genes related to peroxisomal FA oxidation in the porcine liver, thereby changing the overall lipid metabolism in pigs. However, the porcine adipose tissue is rather refractory to regulation of transcripts by dietary FA composition.
Implications
Feeding algal docosahexaenoic acid to pigs for 18 d greatly modifies tissue FA composition, indicating that pigs can utilize algal lipids and deposit the dietary FA into several tissues. Dietary docosahexaenoic acid increased hepatic and adipose tissue docosahexaenoic acid content and reduced the messenger RNA for hepatic, but not adipose tissue, adipocyte determination and differentiation-dependent factor 1, a transcription factor that upregulates lipogenesis. In pigs, adipose tissue is the major FA synthesis site; therefore, dietary docosahexaenoic may only slightly affect overall lipogenesis. Perhaps a higher dietary docosahexaenoic or greater deposition of DHA into adipose tissue is needed to decrease expression of adipocyte determination and differentiation-dependent factor 1 and inhibit FA synthesis.
Footnotes
1 We thank C. M. Liu and A. C. Lin for care and feeding of animals. This work was funded in part by the Council of Agriculture (91AS-1.1.3-AD-U1) and the National Science Council (NSC 91-2313-B-002-405) in Taiwan. 
2 Correspondence: 50, Lane 155, Kee-Long Rd., Sec. 3, Taipei, Taiwan (phone: +8862-2732-7301; fax: +8862-2732-4070; e-mail: sding{at}ntu.edu.tw).
Received for publication July 1, 2003. Accepted for publication November 3, 2003.
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