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Institute of Nutritional Sciences, Martin-Luther-University of Halle-Wittenberg, D-06108 Halle/Saale, Germany
2To whom correspondence should be addressed. E-mail: eder{at}landw.uni-halle.de.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • lactation • lipogenic enzymes • mammary gland • oxidized oil • rats
Oxidized lipids as components of heated or fried foods play an important role in nutrition in industrialized countries. Lipid peroxidation products present in oxidized oils influence animal metabolism in several ways. Recently, we showed that a dietary oxidized oil suppresses gene expression and lowers activities of lipogenic enzymes in the liver of rats and leads to reduced concentrations of triglycerides in liver, plasma, and VLDL (1,2). In lactating animals, the mammary gland also has a high capability of triglyceride synthesis. At peak lactation (d 10–14 of lactation), the mammary gland is the major site of lipogenesis in rats (3). The rate of lipogenesis in the lactating gland is very sensitive to composition and availability of the diet: for example, a high-fat diet decreases the rate of lipogenesis (4), ethanol intake during lactation enhances the rate of lipogenesis (5), and withdrawal of food for 24 h decreases the rate of lipogenesis (6). Recently, it has been shown that trans-fatty acids in the diet reduce the activities of lipogenic enzymes and impair lipid biosynthesis in the mammary gland of lactating rats (7). The effect of dietary oxidized oils on the activities of lipogenic enzymes in the mammary gland has not yet been investigated. The present study was conducted to investigate whether a dietary oxidized oil influences gene expression and activities of lipogenic enzymes in the mammary gland of lactating rats. We also examined the gene expression of sterol regulatory element binding protein-1 (SREBP-1),3 a transcription factor involved in the regulation of gene expression of lipogenic enzymes (8). Biosynthesis of fatty acids by lipogenic enzymes and their subsequent esterification is one important source of milk triglycerides. Medium-chain fatty acids with 6–14 carbon atoms are the main products of fatty acid synthesis in the mammary gland, whereas long-chain fatty acids with 18–22 carbon atoms in the milk derive mainly from triglyceride-rich lipoproteins; fatty acids with 16 carbon atoms derive from both sources (9). An altered rate of fatty acid synthesis in the mammary gland, therefore, is expected to influence the concentration of triglycerides in the milk and the ratio between medium-chain and long-chain fatty acids in milk lipids. We therefore also determined the concentrations of lipids and their fatty acid composition in the milk sampled at peak lactation.
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Diets and feeding.
Throughout the entire experiment, one basal diet was used (see Table 1). Supplementation of minerals and vitamins followed the recommendations made by the ASNS (10) for rat diets. The type of oil (fresh oil vs. oxidized oil) was varied (see below). To adjust the vitamin E content of the diets, the native concentrations of tocopherols of the oils were analyzed. Based on the native concentrations of the oils, diets were supplemented individually with all-rac-
-tocopheryl acetate to reach 50 mg -tocopherol equivalents/kg diet [the biopotency of all-rac--tocopheryl acetate is considered to be 67% of that of -tocopherol (11)].
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Rats received experimental diet for a total of 14 wk. To standardize food intake, a restricted feeding scheme was applied during growth, pregnancy, and lactation, whereby each rat received the same amount of diet. The food intake was 
20% below the voluntary diet intake, as determined in earlier studies. During growth, from wk 4 to 12 of age, the amount of food offered each day was increased continuously from 8 to 12 g. In wk 13 of life, when they were paired with adult male rats, the female rats had free access to the diets. Throughout pregnancy, each rat received 13 g of diet/d. During lactation (from d 1 to 19), the amount of food offered each day was increased continuously; starting from 10 g, the amount was increased every 3–4 d by 5 g, reaching 35 g at the end of the experiment.
Preparation of the test oils.
The basal oil used to prepare the oxidized oil was a mixture of sunflower oil and linseed oil (80:20), which was chosen to supply the rats with sufficient amounts of linoleic acid and -linolenic acid. This oil mixture was poured into a quartz glass beaker and heated at a temperature of 50°C in a drying oven for 16 d. Throughout the heating process, air was continuously bubbled through the oil. This treatment caused a loss of PUFA, a complete loss of tocopherols, and raised the concentrations of lipid peroxidation products in the oil. We planned to equalize the fatty acid composition of the fresh and the oxidized oil. Therefore the fresh oil was composed of a mixture of sunflower oil, linseed oil, and palm oil (73:15:12). The extent of lipid peroxidation of the oxidized oil was determined by assaying the peroxide value (12), the concentration of TBARS (13), the concentration of conjugated dienes (14), the acid values (12), the percentage of total polar compounds (15), and the concentration of total carbonyls (16). To determine the concentrations of lipid peroxidation products of the dietary oils after inclusion in the diets, the oils were extracted from the diets with a mixture of hexane and isopropanol (3:2, v/v) according to Hara and Radin (17). The oxidized oil was stored at -20°C until preparation of the diet.
Sample collection.
At d 14 of lactation, milk samples were collected from the dams. After separation from the pups for 1 h, dams were anesthetized i.m. with ketamine (75 mg/kg body weight) and injected i.m. with 1 IU oxytocin to stimulate the milk flow. Milking was performed at 1000 h with a milking machine. From each rat, 2–3 mL of milk was obtained from all teats within 10 min through below atmospheric pressure. Samples were stored at -20°C until analysis. At d 19 of lactation, the dams were killed by decapitation under light anesthesia with diethyl ether. Blood was collected into heparin-polyethylene tubes and plasma was separated by centrifugation (1,500 x g, 10 min, 4°C). VLDL (
< 1.006 kg/L) were isolated by ultracentrifugation of plasma (900,000 x g, 1 h 30 min, 4°C; Mikro-Ultrazentrifuge, Sorvall Products). Liver and mammary glands were excised and immediately shock frozen in liquid nitrogen. Aliquots of the mammary gland were stored at -80°C for RNA isolation; other samples were stored at -20°C. Aliquots of liver and mammary glands were homogenized in ice-cold 0.1 mol/L phosphate buffer (pH 7.0), containing 5 mmol/L EDTA. Liver and mammary gland homogenates were centrifuged at 600 x g (10 min, 4°C); the supernatants were used for the TBARS assay. Mammary gland homogenates were centrifuged a second time at 105,000 x g (60 min, 4°C) to yield the cytosol fraction.
Analysis.
Concentrations of triglycerides in milk total lipids as well as plasma and VLDL of the dams were determined using an enzymatic reagent kit (VWR International, Cat.-No. 1.14856). The fatty acid composition of dietary oils and milk total lipids was determined by GC as described recently (18). The total lipids of the milk were extracted with chloroform. Concentrations of -, ß-, 
- and 
-tocopherol in dietary oils, liver, and milk were determined by HPLC using a Hewlett-Packard system (HP 1100) according to Coors (19) with modifications described recently (18). Concentrations of TBARS were measured in homogenates of liver and mammary glands using a modified method of Halliwell and Gutteridge (20) as described earlier (18). Concentrations of lipid hydroperoxides (LHP) were measured after a 30-min incubation of methanolic extracts from liver, mammary gland, and milk by using the ferrous oxidation-xylenol orange method (21). The total antioxidative capacity of the milk was measured in diluted probes using a commercially kit (Immundiagnostik), intended for the quantitative determination of antioxidants in plasma. Glucose-6-phosphate dehydrogenase (G6PDH) activity was determined in the cytosol fraction according to Deutsch (22), fatty acid synthase (FAS) activity according to Nepokroeff et al. (23), and acetyl-CoA-carboxylase (AcCx) activity according to Tanabe et al. (24). Activities were related to the protein concentrations of the probes determined by the method of Bradford (25).
For real time RT-PCR analysis, total RNA was extracted from frozen mammary gland tissue using Trizol reagent (Invitrogen) according to the manufacturer’s instructions. RNA integrity was verified by agarose gel electrophoresis using ethidium bromide for visualization. Total RNA (1 µg) was used for cDNA synthesis with 65 U Revert Aid M-MuLV Reverse Transcriptase (MBI-Fermentas) and 0.5 µg oligo dT18 primer (Qiagen-Operon) for 1 h at 42°C followed by an inactivation step of 70°C for 10 min. mRNA expressions of G6PDH, FAS, SREBP-1, and ß-actin as a housekeeping gene for normalization, were determined by quantitative real time RT-PCR, using an MJ OPTICON system (Biozym). 1 µL cDNA was amplified in a total volume of 10 µL using the Brilliant SYBR Green QPCR Master Mix (Stratagene-Europe) and specific primers at 0.25 µmol/L each.
After initial denaturation and activation of the polymerase at 95°C for 10 min, cycling was performed for 40–60 cycles with annealing at 60°C for 20 s, synthesis at 72°C for 30 s, and denaturation at 94°C for 20 sec. Fluorescence was measured at the end of the elongation step at 72°C. Primer oligonucleotides for the G6PDH gene were: 5' primer, 5'-GAG-GGT-CGT-GGG-GGC-TAT-TTT-3'; 3' primer, 5'-TGG-GGT-ACT-GTG-GGG-TCA-TCT-AAG-3'. Primer oligonucleotides for the FAS gene were: 5' primer, 5'-CCT-CTT-CCC-TGG-CAC-TGG-CTA-CCT-3'; 3' primer, 5'-ACT-CGG-CGG-GGA-TCG-GGA-CTT-3'. Primer oligonucleotides for the SREBP-1 gene were: 5' primer, 5'-GGA-GCC-ATG-GAT-TGC-ACA-TT-3'; 3' primer, 5'-AGG-AAG-GCT-TCC-AGA-GAG-GA- 3'. Primer oligonucleotides for the actin gene were: 5' primer, 5'-GTG-GGG-CGC-CCC-AGG-CAC-CA-3'; 3' primer, 5'-GTC-CTT-AAT-GTC-ACG-CAC-GAT-TTC-3'. All primers were obtained from Roth (Karlsruhe, Germany).
Statistical analysis. Means of the two groups of rats were compared by Student’s t test. Results are expressed as means ± SD. Means were considered significantly different at P < 0.05.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Antioxidative status of the rats.
Rats fed the oxidized oil had higher concentrations of TBARS and LHP but lower concentrations of -tocopherol in their livers than rats fed the fresh oil (Table 3). Concentrations of TBARS and LHP in mammary glands of rats fed oxidized oil and those of rats fed the fresh oil did not differ. Concentrations of LHP and -tocopherol and the antioxidant capacity in the milk of rats fed the oxidized oil and those of rats fed the fresh oil also did not differ.
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Relative mRNA concentrations of lipogenic enzymes and SREBP-1 in the mammary gland. The relative mRNA concentration of G6PDH tended to be lower in rats fed the oxidized oil than in rats fed the fresh oil (32.5 ± 15.0 vs. 46.3 ± 19.9% of ß-actin, P < 0.15, n = 7), whereas mRNA concentrations of FAS (0.04 ± 0.05 vs. 0.07 ± 0.07 copies, % of ß-actin, n = 7) and SREBP-1 (75 ± 60 vs. 85 ± 55 copies, % of ß-actin, n = 7) did not differ between rats fed the fresh oil and those fed the oxidized oil.
Concentration of triglycerides in the milk and fatty acid composition of milk total lipids. The milk of rats fed the oxidized oil had lower concentrations of triglycerides than the milk of rats fed the fresh oil (97 ± 50 vs. 204 ± 86 µmol/g, P < 0.05, n = 7). Total lipids in the milk of rats fed the oxidized oil contained more medium-chain saturated fatty acids (C10, C12, C14) and less long-chain monounsaturated fatty acids (16:1, 18:1) than those in the milk of rats fed the fresh oil (Fig. 1). Relative concentrations (mol/100 mol fatty acids) of medium-chain fatty acids (C8-C14) in the milk were higher in the rats fed the oxidized oil, whereas those of fatty acids with 16 carbon atoms (C16) and those of fatty acids with 18–22 carbon atoms (C18-C22) were lower than in rats fed the fresh oil (Table 4). Absolute concentrations (µmol/g) of medium-chain fatty acids were not different between the milk of rats fed the oxidized oil and that of rats fed the fresh oil; the concentrations of fatty acids with 16 carbon atoms and those with 18–22 carbon atoms were lower in the milk of rats fed the oxidized oil than in that of rats fed the fresh oil. The concentrations of elaidic acid (18:1 trans-9) and various conjugated linoleic acid isomers (18:2 cis-9, trans-11; C18:2 trans-10, cis-12; 18:2 trans-9, trans-11) were low and did not differ between the milk of rats fed oxidized oil and that of rats fed fresh oil. The concentration of 18:1 trans-9 was 1.00 ± 0.76 g/100 g fatty acid in rats fed the fresh oil and 0.55 ± 0.15 g/100 g fatty acid in rats fed the oxidized oil; the sum of 18:2 cis-9, trans-11, 18:2 trans-10, cis-12, and 18:2 trans-9, trans-11 was 0.50 ± 0.06 g/100 g fatty acids in rats fed the fresh oil and 0.67 ± 0.16 g/100 g fatty acids in rats fed the oxidized oil (n = 7).
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-tocopherol. Earlier studies also showed that dietary oxidized oils lower the antioxidant capacity and increase lipid peroxidation in the liver of rats (1,2,26,27). The examination of TBARS and LHP in the mammary gland suggests that lipid peroxides from the diet were not readily taken up by the mammary gland. Lipid peroxidation products in the milk are secreted from the mammary gland. The finding that the milk of rats fed the oxidized oil did not contain higher concentrations of lipid peroxidation products and did not have a lower antioxidant capacity than the milk of rats fed the fresh oil is another indication that the mammary gland was not seriously subjected to oxidative stress. In contrast to most of the other studies dealing with the effects of thermoxidized oils (28–30), feeding the diet containing the oxidized oil did not impair the growth of the rats, thus eliminating the possibility that the effects of oxidized oils were confounded by secondary effects of reduced growth. Because the control oil and the oxidized oil were also equalized for their fatty acid composition, we assume that the effects observed in rats fed the oxidized oil were caused predominately by the lipid peroxidation products present in the oxidized oil. It was shown that dietary trans-fatty acids including those with conjugated double bonds such as 18:2 trans-10, cis-12 impair lipid synthesis in the mammary gland (7,31). The oils used in this study had low amounts of trans-fatty acids such as 18:1 trans-9 or conjugated linoleic acids. Consequently, the concentrations of these fatty acids in the milk were also low in both groups of rats. Therefore, we assume that reduced triglyceride concentrations in milk of rats fed the oxidized oil were not caused by dietary trans-fatty acids.
The examination of gene expression and activities ofG6PDH, FAS, and AcCx indicated that dietary oxidized oils did not affect the regulation of lipogenic enzymes in mammary glands of lactating rats. SREBP-1 is a major regulator of de novo lipid synthesis in the lactating mammary gland (32). The finding that gene expression of SREBP-1 was not influenced is another indicator that the dietary oxidized oil did not affect lipogenesis in the mammary gland. Medium-chain fatty acids with 8–14 carbon atoms are the main products of de novo fatty acid synthesis in the mammary gland. The fact that the concentration of medium-chain fatty acids in the milk did not differ between rats fed oxidized oil and those fed fresh oil also indicates that oxidized oils did not inhibit lipogenesis in the mammary gland.
In addition to fatty acids synthesized in the mammary gland, fatty acids released from triglyceride-rich lipoproteins by lipoprotein lipase (LPL) and taken up into the mammary gland are another important source for milk triglyceride synthesis. Those fatty acids largely reflect those of the diet; they are predominately long-chain fatty acids with 18–22 carbon atoms, either saturated or unsaturated (33). The finding that the milk of rats fed the oxidized oil had markedly reduced concentrations of long-chain fatty acids suggests that the oxidized oil impaired the uptake of those fatty acids into the mammary gland, and therefore impaired the synthesis of triglycerides with long-chain fatty acids. Because the concentration of triglycerides in plasma and VLDL were not lower but were even higher in rats fed the oxidized oil than in rats fed the fresh oil, we assume that the activity of LPL, the key factor in the uptake of circulating lipids by the lactating mammary gland (34) could have been reduced. It was shown recently that some lipid oxidation products suppress gene expression of LPL in macrophages (35). The uptake of fatty acids from plasma lipids into the mammary gland depends on the lipid intake. In lactating rats fed diets with high fat concentrations, most of the fatty acids in the milk originated from plasma lipids; lactating rats fed low-fat diets have a relatively high content of fatty acids derived from mammary gland lipogenesis (4). In the present study, a diet with a relatively high fat concentration (100 g/kg) was used. The relatively high concentrations of fatty acids with 18–22 carbon atoms in the milk of rats fed the fresh oil diet confirms that under these conditions most of the milk fatty acids derived from plasma lipids. If the reduction of the triglyceride concentration in the milk by the oxidized oil is caused by a reduced uptake of fatty acids from plasma, this effect might be less pronounced with a low-fat diet or even non existent with an oil-free diet. Further studies are required to investigate the relationship between oxidized oils, LPL, and triglyceride synthesis in the mammary gland.
Recently, it was shown that oxidized frying oils activate the peroxisome proliferator-activated receptor (PPAR) in the liver and stimulate mitochondrial and peroxisomal ß-oxidation of fatty acids, leading to a reduction in hepatic triglyceride concentration (36). We cannot exclude the possibility that oxidized oils also activate PPAR in the mammary gland and stimulate ß-oxidation of fatty acids. Whether such an effect could be at least partially responsible for the reduced triglyceride concentrations in the milk of rats fed an oxidized oil should be investigated in further studies.
In conclusion, our study shows that the intake of an oxidized oil does not reduce the activities of lipogenic enzymes in the mammary gland of lactating rats but lowers the triglyceride concentration in their milk.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: AcCx, acetyl-CoA carboxylase; FAS, fatty acid synthase; G6PDH, glucose-6-phosphate-dehydrogenase; LHP, lipid hydroperoxides; LPL, lipoprotein lipase; PPAR, peroxisome proliferator-activated receptor ; SREBP, sterol regulatory element binding protein.
Manuscript received 16 September 2003. Initial review completed 22 October 2003. Revision accepted 24 November 2003.
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LITERATURE CITED |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Eder, K., Suelzle, A., Skufca, P., Brandsch, C. & Hirche, F. (2003) Effects of dietary thermoxidized fats on expression and activities of lipogenic enzymes in rats. Lipids 38:31-38.[Medline]
2. Eder, K. & Kirchgessner, M. (1998) The effect of dietary vitamin E supply and a moderately oxidized oil on activities of hepatic lipogenic enzymes in rats. Lipids 33:277-283.[Medline]
3. Williamson, D. H. & Da Costa, M. T. (1993) The regulation of lipid metabolism in lactation. Medina, J. M. Quero, J. eds. Physiological Basis of Perinatal Care 1993:63 Ergon Salamanca, Spain. .
4. Del Prado, M., Villalpando, S., Gordillo, J. & Hernandez-Montes, H. (1999) A high dietary lipid intake during pregnancy and lactation enhances mammary gland lipid uptake and lipoprotein lipase activity in rats. J. Nutr. 129:1574-1578.
5. Tavares de Carmo, M. G., Oller Do Nascimento, C. M., Martin, A. & Herrera, E. (1996) Effects of ethanol intake on lipid metabolism in the lactating rat. Alcohol 13:443-448.[Medline]
6. Williamson, D. H. (1990) The lactating mammary gland of the rat and the starved-fed transition: a model system for the study of the temporal regulation of substrate utilization. Biochem. Soc. Trans. 18:853-856.[Medline]
7. Assumpcao, R. P., Santos, F. D., Setta, C. L., Barreto, G. F., Matta, I. E. A., Estadella, D., Azeredo, V. B. & Tavares Do Carmo, M. G. (2002) Trans fatty acids in maternal diet may impair lipid biosynthesis in mammary gland of lactating rats. Ann. Nutr. Metab. 46:169-175.[Medline]
8. Shimano, H., Yahagi, N., Amemiya-Kudo, M., Hasy, A. H., Osuga, J.-I., Tamura, Y., Shionoiri, F., Iizuka, Y., Ohashi, K., Harada, K., Gotoda, T., Ishibashi, S. & Yamada, N. (1999) Sterol regulatory element-binding protein-1 as a key transcription factor for nutritional induction of lipogenic enzyme genes. J. Biol. Chem. 274:35832-35839.
9. Ross, A., Davilla, M. & Clearly, M. P. (1985) Fatty acids and retinyl esters of rat milk. Effects of diet and duration of lactation. J. Nutr. 115:1488-1497.
10. Reeves, P. G., Nielsen, F. H. & Fahey, G. C., Jr (1993) AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet. J. Nutr. 123:1939-1951.
11. Weiser, H. & Vecchi, M. (1982) Stereoisomers of alpha-tocopheryl acetate. II. Biopotencies of all eight stereoisomers, individually or in mixtures, as determined by rat resorption-gestation tests. Int. J. Vitam. Nutr. Res. 52:351-370.[Medline]
12. Deutsche Gesellschaft für Fettwissenschaft (1994) Einheitsmethoden zur Untersuchung von Fetten, Fettprodukten, Tensiden und verwandten Stoffen 1994 Wissenschaftliche Verlagsgesellschaft Stuttgart, Germany.
13. Sidwell, C. G., Salwin, H., Benca, M. & Mitchell, J. H., Jr (1954) The use of thiobarbituric acid as a measure of fat oxidation. J. Am. Oil Chem. Soc. 31:603-606.
14. Recknagel, R. O. & Glende, E. A., Jr (1984) Spectrophotometric detection of lipid conjugated dienes. Methods Enzymol. 105:331-337.[Medline]
15. International Union of Pure and Applied Chemistry (IUPAC) (2000) Determination of polar compounds, polymerized and oxidized triacylglycerols, and diacylglycerols in oils and fats. Pure Appl. Chem. 72:1563-1575.
16. Endo, Y., Li, C. M., Tagiri-Endo, M. & Fujimoto, K. (2001) A modified method for the estimation of total carbonyl compounds in heated and frying oils using 2-propanol as a solvent. J. Am. Oil Chem. Soc. 78:1021-1024.
17. Hara, A. & Radin, S. N. (1978) Lipid extraction of tissues with a low-toxicity solvent. Anal. Biochem. 90:420-426.[Medline]
18. Brandsch, C., Ringseis, R. & Eder, K. (2002) High dietary iron concentrations enhance the formation of cholesterol oxidation products in the liver of adult rats fed salmon oil with minimal effects on antioxidant status. J. Nutr. 132:2263-2269.
19. Coors, U. (1991) Anwendung des Tocopherolmusters zur Erkennung von Fett- und Ölmischungen. Fat Sci. Technol. 93:519-526.
20. Halliwell, B. Gutteridge, J.M.C. eds. Free Radicals in Biology and Medicine 1989 Clarendon Press Oxford, UK. .
21. Hermes-Lima, M., Willmore, W. G. & Storey, K. B. (1995) Quantification of lipid peroxidation in tissue extracts based on Fe(III)xylenol orange complex formation. Free Radic. Biol. Med. 19:271-280.[Medline]
22. Deutsch, J. (1995) Glucose-6-phosphate dehydrogenase. Bergmeyer, H. U. eds. Methods of Enzymatic Analysis 3:190-197 Verlag Chemie VCH, Weinheim, Germany. .
23. Nepokroeff, C. M., Lakshmanan, M. R. & Porter, J. W. (1975) Fatty acid synthase from rat liver. Methods Enzymol. 35:37-44.[Medline]
24. Tanabe, T., Nakanishi, S., Hashimoto, T., Ogiwara, H., Nikawa, J. & Numa, S. (1981) Acetyl-CoA carboxylase from rat liver. Methods Enzymol. 71:5-16.
25. Bradford, M. M. (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal. Biochem. 72:248-254.[Medline]
26. Yoshida, H. & Kajimoto, G. (1989) Effect of dietary vitamin E on the toxicity of autoxidized oil to rats. Ann. Nutr. Metab. 33:153-161.[Medline]
27. Liu, J.-F. & Huang, C.-J. (1995) Tissue -tocopherol retention in male rats is compromised by feeding diets containing oxidized frying oil. J. Nutr. 125:3071-3080.
28. Corcos Benedetti, P., D’Aquino, M., Di Felice, M., Gentili, V., Tagliamonte, B. & Tomassi, G. (1987) Effects of a fraction of thermally oxidized soy bean oil on growing rats. Nutr. Rep. Int. 36:387-401.
29. Blanc, P., Revol, A. & Pacheco, H. (1992) Chronical ingestion of oxidized oil in the rat: effect on lipid composition and on cytidylyl transferase activity in various tissues. Nutr. Res. 12:833-844.
30. Hochgraf, E., Mokady, S. & Cogan, U. (1997) Dietary oxidized linoleic acid modifies lipid composition of rat liver microsomes and increases their fluidity. J. Nutr. 127:681-688.
31. Baumgard, L. H., Matitashvili, E., Corl, B. A., Dwyer, D. A. & Bauman, D. E. (2002) trans-10, cis-12 conjugated linoleic acid decreases lipogenic rates and expression of genes involved in milk lipid synthesis in dairy cows. J. Dairy Sci. 85:2155-2163.
32. Barber, M. C., Vallance, A. J., Kennedy, H. T. & Travers, M. T. (2003) Induction of transcripts derived from Promoter III of the acetyl-CoA carboxylase-alpha gene in mammary gland is associated with recruitment of SREBP-1 to a region of the proximal promoter defined by a DNase-I hypersensitive site. Biochem. J. 375:489-501.[Medline]
33. Green, M. H., Dohner, E. L. & Green, J. B. (1981) Influence of dietary fat and cholesterol on milk lipids and on cholesterol metabolism in the rat. J. Nutr. 111:276-278.
34. Scow, R., Chernick, S. & Fleck, R. (1977) Lipoprotein lipase and uptake of triacylglycerol, cholesterol and phosphatidylcholine from chylomicrons by mammary gland and adipose tissue of lactating rats in vivo. Biochim. Biophys. Acta 487:297-306.[Medline]
35. Hulten, L. M., Lindmark, H., Diczfalusy, U., Bjorkhem, I., Ottosson, M., Liu, Y., Bondjers, G. & Wiklund, O. (1996) Oxysterols present in atherosclerotic tissue decrease the expression of lipoprotein lipase messenger RNA in human monocyte-derived macrophages. J. Clin. Investig. 97:461-468.[Medline]
36. Chao, P.-M., Chao, C.-Y., Lin, F.-J. & Huang, C.-J. (2001) Oxidized frying oil up-regulates hepatic acyl-CoA oxidase and cytochrome P450 4A1 genes in rats and activates PPAR. J. Nutr. 131:3166-3174.
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