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Nutrient Interactions and Toxicity

Thermally Oxidized Dietary Fats Increase Plasma Thyroxine Concentrations in Rats Irrespective of the Vitamin E and Selenium Supply^{1 ,2}

Institut für Ernährungswissenschaften, Martin Luther Universität Halle Wittenberg, D-06108 Halle/Saale, Germany

³To whom correspondence should be addressed. E-mail: eder{at}landw.uni-halle.de.

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
A recent study demonstrated that feeding a diet with a thermally oxidized fat increases the concentration of thyroxine in plasma of miniature pigs. This study was undertaken to investigate whether the effect of thermally oxidized fats on plasma thyroid hormones is influenced by the supply of vitamin E or selenium. Two experiments were conducted using male Sprague-Dawley rats. The first experiment included eight groups of rats fed diets with either fresh fat or three different types of oxidized fat prepared by heating at 50°C, 105°C or 190°C for 42 d. The diets contained either 25 or 250 mg -tocopherol equivalents per kg. The second experiment included four groups of rats fed diets with fresh fat or oxidized fat heated at 55°C, containing either 70 or 570 µg selenium per kg for 56 d. Rats fed all types of oxidized fats had higher concentrations of free and total thyroxine in plasma than rats fed the equivalent diets with fresh oil; the concentrations of triiodothyronine and thyroid-stimulating hormone did not differ between rats fed fresh and those fed oxidized fats. The effect of the oxidized fat on the plasma thyroxine concentration was completely independent of the supply of vitamin E (expt. 1) and the supply of selenium (expt. 2). Our results confirm that oxidized dietary fats raise the plasma thyroxine concentration and show that this phenomenon is independent of the vitamin E and selenium status.

KEY WORDS: • rats • oxidized fat • selenium • vitamin E • thyroxine

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
In developed countries, fried foods are an important source of fat. Thermally oxidized fats contain a large number of lipid peroxidation products that are known to affect animal metabolism in several ways (1 ). Recent studies in miniature pigs demonstrated that feeding diets with thermally treated oils increases the concentration of free and total thyroxine in plasma (2 ,3 ). This finding might be of particular importance because thyroid hormones play crucial roles in energy metabolism and thermogenesis. The mechanism by which oxidized fats raise plasma thyroxine levels is unknown. This study was undertaken to provide further insights into the relationship between oxidized fats and thyroid hormone metabolism.

Most of the deleterious effects of oxidized fats are due to their pro-oxidant effects and can be diminished by increasing dietary vitamin E concentrations (4 ). The effect of oxidized fats on the thyroid hormone metabolism, therefore, could also be due to oxidative stress. If this were the case, a high intake of antioxidants such as vitamin E ought to prevent this effect. The first experiment of this study, therefore, was designed to investigate whether the effect of oxidized fats on plasma thyroxine concentration is influenced by the dietary vitamin E level. Therefore, we conducted an experiment with growing rats fed diets with nutritionally adequate (25 mg/kg) or excess (250 mg/kg) concentrations of vitamin E. We also proposed to study the effect of fats that had been treated in different ways. Heating fats for a long period at low temperatures without catalysts produces mainly primary lipid peroxidation products such as peroxides and hydroperoxides. Because the primary lipoxy radical is unstable, fats treated at high temperatures or in the presence of catalysts contain predominantly secondary lipid peroxidation products such as carbonyls or dimeric, trimeric, polymeric and cyclic fatty acids (5 ). The physiological effects of primary and secondary lipid peroxidation products are different. Primary lipid peroxidation products are highly toxic when administered parenterally but less toxic when given orally, probably due to low digestibility (6 ,7 ). Secondary lipid peroxidation products are of particular physiological importance because they are highly digestible (8 ). To demonstrate possible effects of the oxidized fats, we used diets with high levels of fat (100 g/kg).

The metabolism of thyroid hormones is influenced by several nutritive factors. Selenium as a constituent of type I, iodothyronine 5' deiodinase (5'IDI)⁴ is also involved in the metabolism of thyroid hormones (9 ,10 ). In the selenium-deficient state, the conversion of thyroxine to triiodothyronine by this enzyme is inhibited, and, consequently, the concentration of thyroxine in plasma is higher than under adequate selenium supply (11 –13 ). In chickens, oxidized fats reduce the activity of glutathione peroxidase (GSH-Px) (4 ), an indicator of the selenium status (14 ). This finding suggests that dietary oxidized fats affect the selenium status of animals. A reduced selenium status, leading to a reduced activity of 5'IDI, therefore, could be responsible for the increased plasma thyroxine concentration in animals fed oxidized fats. To ascertain a possible relationship between oxidized fats, selenium status and the metabolism of thyroid hormones in plasma, the second experiment investigated the effect of oxidized fats on the concentrations of thyroid hormones in plasma and the activity of hepatic 5'IDI at various selenium supply levels of rats. To induce very different selenium states, diets with either deficient (70 µg/kg) or excess (570 µg/kg) selenium concentrations were used. Because selenium is stored in body pools during life (15 ), we used in this experiment young rats with an initial body weight of 50 g with low amounts of selenium stored in their body at the beginning of the experiment. Because young rats are more sensitive against deleterious effects of oxidized fats, diets were used with a fat level (50 g/kg) lower than that of the diets in expt. 1.

Experiments using oxidized fats are often hampered by methodological problems. The administration of a diet containing highly oxidized fats reduces food intake, food efficiency and the digestibility of fatty acids (4 ,16 ,17 ). Highly oxidized fats usually contain significantly less polyunsaturated fatty acids (PUFA) and tocopherols than the equivalent fresh oils because of loss through oxidation (16 ,17 ). The effects of dietary lipid peroxidation products, therefore, are confounded by a different nutritional status and different growth rates in treatment and control groups. The nutritional status of animals, in particular, the energy intake, has a marked effect on the release of thyroid hormones from the thyroid gland and the rate of hepatic deiodination (18 ). To avoid these confounding effects, we used moderately oxidized fats and a controlled feeding system in which rats of all treatment groups were given identical amounts of food. Dietary fats were equalized for their fatty acid composition by using mixtures of various fats and tocopherol concentrations of the oils by individual supplementation of fresh and oxidized fats with all-rac--tocopheryl acetate.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Animals.

Two experiments were carried out with male Sprague-Dawley rats supplied by Charles River (Sulzfeld, Germany). Experiment 1 included 80 rats with an initial body weight of 103 (±2, SEM) g, which were assigned to 8 groups of 10 rats each; expt. 2 included 40 rats with an initial body weight of 52 (±1, SEM) g, which were assigned to 4 groups of 10 rats each. The rats were kept individually in Macrolon cages in a room maintained at 23°C and 50–60% relative humidity with lighting from 0600 to 1800 h. All experimental procedures described followed established guidelines for the care and handling of laboratory animals and were approved by the council of Saxony-Anhalt.

Diets.

Purified diets were used (Table 1) . The composition of the diets was similar in both experiments. The concentration of fat was 100 g/kg in expt. 1 and 50 g/kg in expt. 2. The diets contained sufficient amounts of minerals and vitamins based on recommendations by the American Institute of Nutrition (19 ) for rat diets. The concentrations of vitamin E (expt. 1) and selenium (expt. 2) were selected in accordance with the experimental design.

In expt. 2, the type of fat (fresh fat vs. oxidized fat, see the Preparation of the fats section) and the selenium concentration (low selenium vs. high selenium) were varied. The low selenium diet contained 70 µg selenium as native selenium of the dietary components; high selenium diets were supplemented with 500 µg selenium per kg diet as sodium selenite pentahydrate (supra pure quality; Merck, Darmstadt, Germany).

Diets were prepared by mixing the dry components with the fat and water and subsequent freeze drying. The residual water content of the diet was below 5 g/100 g of diet.

In both experiments, food was administered in restricted amounts to standardize intake. Rats were fed once daily at 0800 h. The amount of food administered was 20% less than the amounts of identical diets with fresh fats consumed ad libitum by rats in preliminary studies. The amount of food offered daily was increased continuously during the experiment from 8.3 g to 17.4 g (expt. 1) and from 8.0 g to 18.3 g (expt. 2). In this feeding system, the food offered was completely consumed by all the rats. Thus, all the rats within one experiment consumed identical amounts of food. Water was freely available from nipple drinkers. The experimental diets were fed for 42 d in expt. 1 and for 56 d in expt. 2.

Preparation of the fats.

In expt. 1, a fresh fat consisting of a mixture of sunflower oil and lard (31:69) and three different types of oxidized fats consisting of mixtures of sunflower oil and lard (1:1) were used. The first type was prepared by heating for 38 d at 50°C; the second type of oxidized fat was prepared by heating for 81 h at 105°C; the third type of the oxidized fat was prepared by heating for 24 h at 190°C. In expt. 2, the fresh fat consisted of a mixture of sunflower oil and lard (4:1). The oxidized fat used in expt. 2 was prepared by heating sunflower oil at 55°C for 42 d. For heat treatment, the fats were filled into quartz glass beakers that were placed into a drying oven set at the intended temperature. Throughout the heating process, air was continuously bubbled through the fats. This treatment caused a loss of PUFA, a complete loss of tocopherols and raised the concentrations of lipid peroxidation products in the fats. We equalized the fatty acid composition of fresh and oxidized fats by varying the ratio of lard to sunflower oil in the fat mixtures. The extent of lipid peroxidation was determined by assaying the peroxide value (POV) (20 ), concentration of thiobarbituric acid-reactive substances (TBARS) (21 ), concentration of conjugated dienes (22 ), acid values (23 ) and the percentage of total polar compounds (24 ).

Sample collection.

After completion of the feeding periods, the rats were starved for 12 h and killed by decapitation under light anesthesia with diethyl ether. Blood was collected into heparinized polyethylene tubes. The liver was excised. Plasma was obtained by centrifugation of the blood (1100 x g, 10 min). Plasma and liver were stored at -20°C. In expt. 1, feces of the rats were collected for 5 d during wk 4 and 6 to determine the digestibility of -tocopherol (during wk 4 and 6).

Analytical methods.

Plasma concentrations of total and free thyroxine and total triiodothyronine were measured with radioimmunoassay kits from ICN Pharmaceuticals, Inc. (Costa Mesa, CA; Cat-No. 06B-254011, -257214, -254215). The concentrations of thyroid-stimulating hormone (TSH) were determined with a commercial radioimmunoassay test kit for rats (Biocode, Liege, Belgium; Rat TSH AH R001). The intra-assay CV were 4.3% for total thyroxine, 3.9% for free thyroxine, 5.4% for triiodothyronine and 2.9% for TSH.

The selenium concentration of the liver was measured after wet-ashing of liver samples with a mixture of 65% nitric acid, 30% hydrochloric acid, 70% perchloric acid (2:1:1, v/v/v) on an atomic absorption spectrophotometer equipped with a graphite tube system (HGA-500; Perkin-Elmer, Überlingen, Germany).

The activity of glutathione peroxidase in plasma was determined by the method of Paglia and Valentine (25 ). The activity of hepatic 5'IDI was measured according to a method of Chopra et al. (26 ). Liver tissue was homogenized in ice-cold 0.1 mol/L phosphate buffer (pH 7.0), containing 5 mmol/L ethylene diamine tetra acetic acid. The supernatant after centrifugation (600 x g, 10 min, 4°C) was diluted to a known protein concentration with buffer and used for assaying the conversion of thyroxine to triiodothyronine. Thyroxine (50 µL) solution (15 µmol/L thyroxine; Merck; in 5 mmol/L sodium hydroxide) and 100 µL of the homogenate were added to 350 µL of buffer. The reaction mixture was incubated at 37°C for 10 min. The reaction was stopped by addition of 1 mL ethanol. Triiodothyronine generated was extracted into ethanol. After centrifugation (1100 x g, 4°C, 10 min), the amount of triiodothyronine was determined by radioimmunoassay as descried above. Each sample was run in duplicate. The results were corrected for origin triiodothyronine and the nonenzymatic conversion of thyroxine into triiodothyronine. The intra-day CV was 5.4%.

The fatty acid composition of the experimental fats was determined by gas chromatography. Fats were transmethylated into fatty acid methyl esters (FAME) with trimethylsulfonium hydroxide. FAME were separated by gas chromatography using a gas chromatographic system (HP 5890; Hewlett-Packard, Taufkirchen, Germany) fitted with an automatic on-column injector, a flame ionization detector and a polar capillary column (FFAP, 30 m, 0.53-mm internal diameter; Macherey and Nagel, Düren, Germany). FAME were detected by flame ionization and identified by comparing their retention times with those of individually purified standards (27 ).

Concentrations of individual tocopherols in plasma, liver, feces and oils were determined by HPLC (28 ). Samples were mixed with 1 mL of 1% pyrogallol solution (in ethanol, absolute) and 150 µL of saturated sodium hydroxide solution. This mixture was heated for 30 min at 70°C, and tocopherols were extracted with n-hexane. Individual tocopherols of the extracts were separated isocratically using a mixture of n-hexane and 1,4 dioxane (96:4, v/v) as mobile phase and a LiChrosorb Si 60 column (5-µm particle size, 250-mm length, 4-mm internal diameter; Merck) and detected by fluorescence (excitation wavelength: 295 nm; emission wavelength: 320 nm).

Statistics.

Results of both experiments were treated by two-way ANOVA. For statistical significant F values, individual means were compared by Fisher’s multiple range test. Means were considered significantly different at P < 0.05.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Characterization of the experimental fats.

Some characteristics of the fats used in expt. 1 are shown in Table 2 . The fatty acid composition was similar in the fresh fat and the three different types of oxidized fats. Before inclusion into the diet, the POV of the oxidized fat treated at 50°C was 500 times higher, that of oxidized fat treated at 105°C was nearly 100 times higher and that of oxidized fat treated at 190°C was twice that of the fresh fat. The percentages of total polar compounds were similar in all three types of oxidized fats. In the fats treated at 50°C, 105°C and 195°C, they were 20, 22 and 17 times higher, respectively, than in the fresh fat. Inclusion of the fats into the diet increased the POV of all fats. After inclusion into the diet, the POV of oxidized fats treated at 50°C, 105°C and 190°C were 200, 50 and 9 times higher, respectively, than that of the fresh oil. The TBARS levels rose even more sharply, with concentrations 2000, 200 and 20 times higher in oxidized fats treated 50°C, 105°C and 190°C, respectively, than in the fresh fat. The concentrations of conjugated dienes were similar in oxidized fats treated at 50°C and 105°C, being nearly double that of oxidized fat treated at 190°C and 20 times higher than in the fresh oil. The calculated concentrations of -tocopherol equivalents were the same in all types of oil.

The food consumption throughout the whole feeding period was identical for each rat in the experiment, averaging 14.3 g/d. Body weight gains of the rats were influenced by both factors, dietary fat and vitamin E supply (Table 4) . Rats fed low vitamin E diets with oxidized fats treated at 50°C or 190°C had significantly lower body weight gains than rats fed diets with fresh fat or oxidized fat treated at 105°C. Within the groups fed oxidized fats, rats fed the high vitamin E diets had slightly greater body weight gains than rats fed the low vitamin E diets. Within the groups fed the high vitamin E diets, final body weights did not differ between the control group and the groups fed the different types of oxidized fat.

Feeding diets with oxidized fats increased the concentrations of total and free thyroxine in the plasma regardless of the tocopherol concentrations of the diet. Rats fed diets with oxidized fat treated at 105°C had the highest concentrations of total and free thyroxine in plasma (+17% and +26%, respectively, relative to control rats fed the fresh fat), followed by rats fed diets with oxidized fat treated at 50°C (+10% and +15%, respectively, relative to control rats). Of the oxidized fats tested, the fat treated at 190°C had the weakest effect on the concentration of total and free thyroxine (+5% and +12%, respectively, relative to control rats). The concentrations of triiodothyronine also tended to be higher in the rats fed the oxidized fats treated at 105°C or 190°C than in rats fed the fresh fat (P < 0.10). The concentration of TSH did not differ among the eight treatment groups.

Effect of oxidized fats at various dietary selenium concentrations (expt. 2).

Food consumption over the whole feeding period averaged 16.9 g/d in all rats. At the end of the feeding period, weights of the rats did not differ among groups (Table 5) . Body weight gains were not influenced either by the fat source or by the dietary selenium concentration. The rats fed the high selenium diets had higher concentrations of selenium in liver and plasma and a higher activity of GSH-Px in plasma than rats fed the low selenium diets.

Feeding diets with oxidized fats markedly increased the concentrations of free and total thyroxine, regardless of the rats’ selenium supply. At the two dietary selenium levels, the concentrations of free and total thyroxine were on average 54% and 33% higher, respectively, in rats fed the oxidized fat than in rats fed the fresh fat. The concentrations of triiodothyronine and TSH did not differ among the groups.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Feeding diets with thermoxidized fats raised the concentrations of free and total thyroxine in plasma of rats. This effect was observed in two independent experiments with rats of different ages, different feeding periods, different basal diets, different types of oxidized fats and different concentrations of the fat in the diets. The finding of this study confirms recent studies performed in miniature pigs (2 ,3 ).

When investigating the effects of oxidized fats, special consideration must be given to the treatment of the fat because the formation of primary and secondary lipid peroxidation products depends on the treatment conditions. This study included fats treated at a low temperature over a long time and others treated at a high temperature for a short time. A definite characterization of the concentrations of primary and secondary lipid peroxidation products in thermally treated fats is not easy because of the large number of different products, most of which are unstable and decompose during heating and storage (29 ). To provide a rough estimate of the fats used, we measured the POV and the concentrations of conjugated dienes and TBARS and the percentage of total polar compounds in the fats. The fat treated for a long period at a low temperature had a high POV, and high concentrations of TBARS and conjugated dienes. Therefore, we assumed that the diets with fats treated at low temperature had high concentrations of primary lipid peroxidation products. By contrast, the fat treated at a high temperature had a much lower POV and lower concentrations of TBARS and dienes than the fat treated at the lower temperature. This might be due to the fact that a large proportion of the relatively volatile lipid peroxidation products is stripped from the fat by air at the high temperature and a virtual steady state is reached between their production and removal from the system. The percentages of polar compounds were high in both fats treated at low temperature and those treated at high temperature. Because those compounds are formed primarily during later stages of lipid peroxidation, we assumed that the concentrations of secondary lipid peroxidation products were high in all the oxidized fats used in this study.

In several studies, feeding diets with oxidized oils reduced the growth in animals due to oxidative stress and a reduced digestibility of nutrients (4 ,14 ,30 ,31 ). In our studies, feeding oxidized fats did not markedly affect body weights of the rats. This indicates that the fats used in our study were moderately oxidized compared with those used in other studies and did not produce general toxic effects in the rats. Only in expt. 1 was a small reduction in body weight gains due to the oxidized oil found when the dietary vitamin E concentration was relatively low. Because an increase in the dietary vitamin E concentration from 25 to 250 mg -tocopherol equivalents per kg prevented growth reduction, we assume that the growth depression might be attributed to oxidative stress induced by the oxidized oil. Other studies also found that increasing the dietary vitamin E concentration reduced the deleterious effects of oxidized fats (4 ). Unlike expt. 1, there was no adverse effect of the oxidized fat on growth of the rats in expt. 2. This might be predominately due to the lower concentration of the oxidized oil in the diets of expt. 2 compared with expt. 1.

In expt. 1, the strongest effect on the concentrations of thyroxine was not caused by the oxidized fat treated at 50°C, which had the highest POV and TBARS concentrations, but by oxidized fat treated at 105°C. This suggests that the effects of oxidized fats on thyroid hormone metabolism might be determined not only by primary but also by secondary lipid peroxidation products. Because the effect of oxidized fats on thyroxine concentrations was completely independent of the dietary vitamin E concentration, that effect likely is not primarily due to general oxidative stress induced by consuming diets with oxidized fats. Oxidative stress is generally associated with increased peroxidation of membrane PUFA and formation of lipid peroxidation products. Tocopherols, which are incorporated into the membrane structure, can prevent the formation of lipid peroxides (32 ). If peroxides originating either from the diet or from endogenous lipid peroxidation were involved in raising the plasma thyroxine concentration, this effect would be expected to be reduced by higher tissue tocopherol concentrations. Rats fed the oxidized fat diet with high vitamin E had 2–5 times higher concentrations of tocopherols in liver and plasma than rats fed the oxidized fat diet with low vitamin E. However, the concentrations of thyroxine in plasma were similar in both groups of rats.

The finding that feeding oxidized oils lowers the vitamin E concentrations in plasma and tissues agrees with several other studies (17 ,33 ). Besides an enhanced utilization of vitamin E by endogenous lipid peroxidation (17 ), we found that a reduced digestibility of tocopherols from the intestine caused by oxidized fats contributes to the reduced tissue vitamin E concentration.

As a constituent of 5'IDI, selenium plays an important role in the metabolism of thyroid hormones (9 –11 ). In a previous article, we speculated that increased concentrations of thyroxine observed in miniature pigs fed oxidized fats could be the result of a reduced deiodination of thyroxine to triiodothyronine (2 ). Feeding oxidized fats did reduce the selenium status of rats as indicated by selenium concentrations and activity of GSH-Px. The activity of hepatic 5' IDI and plasma concentrations of thyroxine, however, was independent of the selenium status of the rats. These findings clearly show that the elevation of plasma thyroxine concentration by feeding oxidized fats was not due to a reduction of the selenium status of the rats.

This study suggests that a dietary selenium concentration of 70 µg/kg was sufficient for maximum activity of hepatic 5'IDI, whereas higher dietary selenium concentrations are required for maximum activity of hepatic GSH-Px. This finding agrees with another study that demonstrated that those selenoenzymes are differentially regulated (12 ).

Based on the results of this study, it is not possible to explain the effects of oxidized fats on the metabolism of thyroid hormones. Thyroxine is synthesized in thyroid epithelial cells and released from the thyroid into the blood under the control of TSH. Elevated concentrations of thyroxine, as found in hyperthyreosis, normally cause a reduction of the concentration of TSH in plasma via a negative feedback mechanism (34 ). In rats fed oxidized fats, an increase in the plasma thyroxine concentration, however, did not cause reduced concentrations of TSH; this suggests that the mechanism which regulates the release of thyroid hormones from the thyroid by TSH is disturbed. In clinical hyperthyreosis, the plasma concentration of thyroxine is increased along with that of triiodothyronine (34 ). The finding that the concentration of triiodothyronine was not increased in rats fed oxidized fats suggests that there was no increased rate of deiodination of thyroxine into triiodothyronine in peripheral cells. Although thyroxine is far less biologically active than triiodothyronine, increased concentrations of free thyroxine in blood might have important effects on energy metabolism and oxygen consumption. Additional studies are necessary to ascertain the consequences of increased plasma thyroxine concentrations through oxidized fats and to explain the molecular mechanisms underlying this phenomenon.

	FOOTNOTES

 
¹ Presented in part in poster form at the 17th International Congress of Nutrition, Vienna, September 2001 (Eder, K., Skufca, P., Brandsch, C., Hirche, F. & Stangl, G. I. (2001) Dietary oxidized lipids stimulate the thyroid function in pigs and rats. Ann. Nutr. Metab. 45(suppl. 1): 83 (abs.).

² Supported by a grant from the Deutsche Forschungsgemeinschaft (DFG).

⁴ Abbreviations used: GSH-Px, glutathione peroxidase; 5'IDI, type I, iodothyronine 5'deiodinase; POV, peroxide value; PUFA, polyunsaturated fatty acids; TBARS, thiobarbituric acid-reactive substances; TSH, thyroid-stimulating hormone.

Manuscript received 2 November 2001. Initial review completed 4 January 2002. Revision accepted 4 March 2002.

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