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* Forschungs- und Studienzentrum für Veredelungswirtschaft Weser/Ems, Georg-August-Universität Göttingen, D-49377 Vechta, Germany and ** Institut für Ernährungswissenschaften, Technische Universität München-Weihenstephan, D-85350 Freising, Germany
1To whom correspondence should be addressed.
 |
ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • miniature pigs • oxidized oil • thyroid hormones • cholesterol • lipoproteins
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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) and pigs (Eder and Kirchgessner 1997a
)
to result in higher concentrations of plasma triiodothyronine
(T3)2
than fats with predominantly saturated fatty acids such as lard or beef
tallow. In developed countries, fried foods are an important source of
fat. Thermally oxidized fat is generally considered to contain
potentially toxic lipid peroxidation products and to induce oxidative
stress in animals (Kubow 1992
). The literature contains
some indication that oxidative stress could influence thyroid hormone
metabolism (Gupta et al. 1997
). Although the effects of
oxidized fats on animal metabolism have been well characterized,
studies about potential effects of oxidized fats on thyroid hormone
metabolism in animals are lacking. This study therefore aimed to
clarify whether dietary oxidized oils may also affect thyroid hormone
metabolism.
Concentrations of plasma thyroid hormones influence the concentration
of cholesterol in plasma and lipoprotein fractions (Field et al. 1986
, Tanis et al. 1996
). The concentrations of
cholesterol in plasma and lipoproteins are of particular physiologic
importance because they greatly influence the risk of coronary heart
disease in humans. The susceptibility of LDL lipids to peroxidation is
another factor which plays an important role in the development of
atherosclerosis. Although it has been demonstrated that oxidized
dietary lipids accelerate the development of atherosclerosis in
cholesterol-fed rabbits (Strapans et al. 1996
),
there are no definitive data on the effects of dietary oxidized lipids
on plasma cholesterol and the susceptibility of lipoproteins to lipid
peroxidation. The measurement of cholesterol in plasma and lipoproteins
and the susceptibility of plasma lipids to peroxidation were therefore
included in this study.
Miniature pigs were used as an animal model because they reflect human
physiology, especially lipid metabolism, more closely than most other
animal models (Barth et al. 1990
). In studies
investigating the effects of dietary lipid peroxidation, special
consideration must be given to the treatment of the fat used for
oxidation. Autoxidation at low temperatures favors the formation of
primary lipid peroxidation products while heating at high temperatures
and supplementation of metal catalysts favors the formation of
secondary lipid peroxidation products. Because lipid peroxidation
products in Western diets derive mainly from heated and fried products
rather than from autoxidized oil, we used a thermoxidized oil.
Experiments using oxidized fats often have methodological problems. The
administration of a diet containing highly oxidized fats reduces food
intake, food efficiency and the digestibility of fatty acids
(Blanc et al. 1992
, Borsting et al. 1994
,
Corcos Benedetti et al. 1987
, Hayam et al. 1993
, Hochgraf et al. 1997
, Liu and Huang 1996
, Yoshida and Kajimoto 1989
). Highly
oxidized oils usually contain significantly less polyunsaturated fatty
acids (PUFA) and tocopherols than the equivalent fresh oils because of
loss through oxidation (Blanc et al. 1992
,
Borsting et al. 1994
, Corcos Benedetti et al. 1987
, D’Aquino et al. 1985
, Hayam et al. 1995
, Hochgraf et al. 1997
, Liu and Huang 1995
). The effects of dietary lipid peroxidation products on
metabolic variables are therefore confounded by a different nutritional
status and different growth rates in treatment and control groups as
well as a different fatty acid composition of dietary lipids. The
nutritional status of animals, in particular the energy intake, has a
pronounced effect on the release of thyroid hormones from the thyroid
gland and the rate of hepatic thyroxine deiodination (Katzeff et al. 1990
). To avoid these confounding effects, we used a
controlled feeding system and equalized dietary fats for their fatty
acid composition by using mixtures of various fats and tocopherol
concentrations of the oils by individual supplementation of both fats
with all-rac-
-tocopherol acetate. This study, unlike most others,
therefore shows the effects of an oxidized oil in pigs at identical
fatty acid and vitamin E intake compared with control pigs fed diets
with fresh oil.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Sixteen male Göttingen Miniature pigs, bred in our animal facility from a strain supplied by the Institut für Tierzucht und Haustiergenetik, Universität Göttingen, Germany, were used. They weighed between 19.0 and 22.5 kg. They were individually housed in a room maintained at 23°C and 50 to 60% relative humidity with light from 0600 to 1800 h. The day before the beginning of the experimental feeding period, all pigs were weighed and allocated to two groups with body weights of 21.8 ± 0.3 kg (control group) and 22.0 ± 0.3 kg (treatment group).
All experimental procedures described followed established guidelines for the care and use of laboratory animals and were approved by the veterinary office in Vechta, Germany.
Diets.
In the 4 wk before the experiment ("pre-period") all pigs were fed
345–395 g of a nutritionally adequate diet based on conventional
feedstuffs, according to the maintenance energy requirement, which is
0.45 MJ metabolizable energy x kg body weight-0.75
(Table 1
). During the experimental phase, all pigs received 325–400 g of a diet
supplemented with 15% of either fresh or thermoxidized oil. The amount
of food given was individually calculated to provide an energy supply
that was 20% in excess of the maintenance requirement. The pigs were
fed two equal meals at 0800 and 1600 h and had free access to
water throughout the day. The experimental diets were administered for
35 d.
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The thermoxidized oil was prepared by the following procedure: 30 kg of
sunflower oil was poured into a cast iron wok and heated for 48 h
on a hotplate set at a constant temperature of 110°C. Throughout the
heating process, air was continuously bubbled through the oil. The
extent of peroxidation was determined by assaying the peroxide value
(POV; AOAC 1990
) and the concentration of thiobarbituric
acid-reactive substances (TBARS; Sidwell et al. 1954
). This treatment caused a loss of PUFA (from 66.8 to
63.8 g per 100 g total fatty acids of the oil), a complete
loss of tocopherols and an elevation of the POV and concentration of
TBARS (Table 2
). We proposed to equalize the fatty acid composition and the tocopherol
concentrations of both fats. The fat mixture of the control diet was
therefore composed of sunflower oil and lard in a ratio of 94:6
(wt/wt). This fat mixture had a similar fatty acid composition as the
oxidized oil. The heat treatment caused a complete loss of vitamin E.
Vitamin E concentrations were adjusted to the same level by
supplementing the oxidized oil with all-rac--tocopheryl acetate
(considering that the biopotency of all-rac--tocopheryl acetate is
67% of that of -tocopherol).
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At the end of the feeding period, the pigs were food-deprived for 12 h, and blood was taken from the jugular vein following mild anesthesia with intravenous ketamine (40 mg/kg). The blood was collected into heparinized polyethylene tubes. Plasma was prepared by centrifuging the blood (1,100 x g, 10 min). Plasma concentrations of total and free thyroxine (T4) and T3 were measured by radioimmunoassay kits from ICN Pharmaceuticals, Inc. (Costa Mesa, CA; Cat-No. 06B-254011, -257214, -254215, -258709). The concentrations of thyroid hormone-stimulating hormone (TSH) were determined by a commercial radioimmunoassay test kit for human TSH (ICN; Cat. No. 06B-264125) because a kit for the measurement of TSH in pigs was not available. The TSH concentrations obtained should be evaluated as relative values because of the lack of a pig TSH standard. The cross-reactivity was not determined.
Plasma lipoprotein fractions were separated by stepwise
ultracentrifugation (230,000 x g, 20 h, 8°C).
Plasma densities (
) were adjusted by the addition of potassium
bromide. The lipoprotein classes (VLDL, <1.019 kg/L; LDL, 1.019
< < 1.063 kg/L; HDL, 1.063 < < 1.21
kg/L) were removed from each tube by suction with a pipette
(Tiedink and Katan 1989
). The concentrations of total
cholesterol in plasma and lipoprotein fractions were measured
enzymatically using an autoanalyzer (model EPOS; Eppendorf, Hamburg,
Germany) and a commercially available kit reagent (ref. 1489232;
Boehringer, Mannheim, Germany).
The susceptibility of plasma total lipids to lipid peroxidation was
determined according to a modification of the method of Kontush et al. (1997)
. Plasma (5 µL) was diluted with 995 µL of a
solution containing 50 µmol/L of copper sulfate pentahydrate. The
formation of conjugated dienes during incubation was followed by
continuously monitoring the increase in absorbance at 234 nm. For the
calculation of diene concentrations, an extinction coefficient234
nm of 29,500 L x mol-1 x cm-1 was used.
For the analysis of fatty acids in diet and LDL samples, lipids were
extracted with a chloroform/methanol mixture (2:1, v/v) according to
Folch et al. (1957)
. Fatty acids were converted to
methyl esters by transesterification with boron fluoride/methanol
reagent (Morrison and Smith 1964
). Fatty acid methyl
esters were separated by gas chromatography using a gas chromatographic
system (model 3400; Varian; Darmstadt, Germany) fitted with a automatic
split injection system, a flame-ionization detector and a
CP-Sil 88 capillary column (50 m x 0.25 mm internal diameter,
film thickness 0.2 µm; Chrompack, Middleburg, The Netherlands). Fatty
acid methyl esters were identified by comparing their retention times
with those of individual purified standards and quantified with
heptadecanoic acid methyl ester as an internal standard (Eder and Kirchgessner 1996
).
Concentrations of individual tocopherols in plasma, LDL and diets were
determined by HPLC (Balz et al. 1993
). Plasma samples
(100 µL) 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, Darmstadt
Germany) and detected by fluorescence (excitation wavelength: 295 nm;
emission wavelength: 320 nm).
Total protein, albumin, creatinine, urea, glucose, triglycerides, phospholipids, aspartate amino transferase (ASAT, EC 2.6.1.1), alanine amino transferase (ALAT, EC 2.6.1.19), and lactate dehydrogenase (LDH, EC 1.1.1.28) in plasma were determined by standardized procedures using an autoanalyzer (Hitachi 704; Boehringer) and Boehringer kit reagents.
The osmotic fragility of erythrocytes was determined according to the
method of O’Dell et al. (1987)
.
Statistics.
For statistical evaluation, means of the two dietary treatments were compared by Student’s t test. Values in the text are means ± SEM.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Body weights of the pigs fed the control diet and the diet containing the oxidized oil did not differ at the end of the experimental phase (Control: 23.8 ± 0.5 kg, oxidized oil: 24.1 ± 0.5 kg). There were no differences between groups in the activities of marker enzymes of cell damage (overall means ± SEM, n = 16; ASAT; 31.3 ± 3.5 U/L, of both groups; ALAT, 32.3 ± 1.5 U/L; LDH, 728 ± 40 U/L) and the plasma concentrations of total protein (70.5 ± 1.9 g/L), albumin (44.4 ± 0.8 g/L), creatinine (111 ± 8 mol/L), urea (2.18 ± 0.19 mmol/L), glucose (5.41 ± 0.39 mmol/L), triglycerides (0.19 ± 0.03 mmol/L) and phospholipids (1.28 ± 0.10 mmol/L). The osmotic fragility of erythrocytes, which is increased in the presence of oxidative stress, did not differ between the two groups (data not shown).
Plasma thyroid hormone concentrations.
Pigs fed the oxidized oil had greater concentrations of total and free
T4 in plasma than pigs fed the fresh oil (Table 3
). The concentrations of T3 did not differ between the two
groups. Hence, pigs fed the oxidized oil had a higher ratio of
T4 to T3 than pigs fed the fresh oil. The
concentration of TSH tended to be higher in pigs fed the oxidized oil
than in pigs fed the fresh oil (P < 0.10).
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Pigs fed the oxidized oil had lower concentrations of cholesterol in
plasma, HDL and LDL than pigs fed the fresh oil (Table 4
). The reduction of cholesterol due to the oxidized oil was similar in HDL
and LDL. The relationship between cholesterol in HDL and LDL did
therefore not differ between the two groups of pigs (3.07 ± 0.10
vs. 2.91 ± 0.12 in pigs fed oxidized oil and pigs fed fresh oil).
There were significant negative correlations between the concentrations
of free thyroxine and cholesterol (r = -0.40,
P < 0.01, Fig. 1
) and between total thyroxine and cholesterol (r = -0.29, P < 0.05).
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Pigs fed the oxidized oil had lower concentrations of total tocopherols
in the plasma and LDL fraction than pigs fed the control diet
(Table 5
). In spite of this, the susceptibility of plasma lipids to lipid
peroxidation during incubation with copper ions did not differ between
the two groups (Fig. 2
). The fatty acid composition of LDL, an important determinant of the
susceptibility of LDL lipids to peroxidation, did not differ between
the two groups (data not shown).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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).
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 peroxidation products depends on the conditions
during treatment. Autoxidation of PUFA at low temperatures without
catalysts causes mainly primary lipid peroxidation products such as
peroxides and hydroperoxides. These products are highly toxic when
administered parenterally but less toxic when given orally, probably
due to low digestibility (Findlay et al. 1970
,
Kanazawa et al. 1985
). From a practical point of view,
because of the prevalence of heated and fried foods in Western diets,
fats that are subjected to high temperatures are more relevant than
autoxidized oils. We therefore prepared the dietary oxidized oil by
heating sunflower oil at the relatively high temperature of 110°C.
This temperature, however, is far below temperatures used to fry foods.
At the high temperature used for the preparation of the oxidized oil,
the primary lipoxy radical is unstable and large quantities of
secondary products such as aldehydes or ketones might have been formed
(Chang et al. 1978
). These products are of particular
physiologic importance because they are highly digestible
(Oarada et al. 1986
). However, a large portion of
relatively volatile peroxidation products are stripped from the oil by
air at the high temperature, and a virtual steady state is reached
between their production and removal from the system. Furthermore, high
temperatures may induce extensive polymerization and cyclization of
fatty acids in the oil. This might have contributed to the relative
absence of adverse effects by the oxidized oil in this study on weight
gains, plasma clinicochemical variables or osmotic fragility of
erythrocytes. Other studies showed reduced food intakes and body weight
gains as well as some toxic symptoms such as increased tissue weights,
histopathological lesions or increased rate of hemolysis in animals fed
highly autoxidized or thermoxidized oils (Engberg and Borsting 1994
, Huang et al. 1988
, Yoshida and Kajimoto 1989
). The oil used in this study can be considered
moderately oxidized compared with those used in most other studies of
oxidized fats. To quantify the degree of lipid peroxidation in
the oil, we measured POV and TBARS concentrations. These measurements
revealed that the oxidized oil contained 60- to 70-fold higher
concentrations of primary and secondary lipid peroxidation products
than the fresh oil. However, these data are relatively unspecific for
lipid peroxidation products and therefore do not provide specific
information about the lipid peroxidation products of the oil.
The supply of antioxidants also needs to be considered when
interpreting the results because potential detrimental effects of
oxidized dietary lipids are diminished by high vitamin E levels
(Yoshida and Kajimoto 1989
). The requirement for vitamin
E, the most important dietary antioxidant, depends on the amounts of
PUFA in the diet. According to the recommendations of Muggli (1994)
, the vitamin E needed in the basal diet was 53 mg
-tocopherol equivalents per kg. Thus, the vitamin E supply of 87 mg
of -tocopherol equivalents per kg in this study was sufficient. The
vitamin E status as measured by the concentrations of -tocopherol in
plasma and LDL was reduced by feeding the oxidized oil although control
and oxidized oils were equalized for their vitamin E levels. This
agrees with results of other studies demonstrating adverse effects of
dietary lipid peroxidation products on the vitamin E status of animals.
A reduced vitamin E status might be the consequence of an enhanced
turnover or catabolism of tocopherols (Corcos Benedetti et al. 1987
, D’Aquino et al. 1985
, Eder and Kirchgessner 1997b
, Liu and Huang 1995
,
Liu and Huang 1996
). Besides an enhanced
decomposition of tocopherols by radical-induced oxidation, a
reduced absorption of tocopherols could also contribute to the lower
tissue tocopherol concentrations in rats fed the oxidized oils
(Liu and Huang 1995
).
This study demonstrates that a dietary oxidized oil increases the
concentrations of free and total T4 in the plasma. This
effect might be due to an increased release of that hormone from the
thyroid gland. The finding that the concentration of TSH was also
slightly increased in pigs fed the oxidized oil suggests that lipid
peroxidation products do not exert their effect in the thyroid gland
tissue but instead affect the thyrotropic axis. If lipid peroxidation
products had a direct effect on the thyroid gland, reduced TSH
concentrations would be expected as part of a negative feedback
response. Interestingly, the hormonal pattern observed in pigs fed the
oxidized oil (increased concentrations of total and free T4
and TSH and an increased ratio of T4 to T3) was
similar to that observed recently in selenium-deficient rats
(Ruz et al. 1999
). Selenium is an integral part of type
I, 5 deiodinase (Arthur et al. 1990
), but also of
glutathione peroxidase, which is involved in the degradation of
hydroperoxides. Some studies have demonstrated that dietary sources of
highly unsaturated fatty acids such as fish oil increase the activity
of glutathione peroxidase (Bellisola et al. 1992
,
Olivieri et al. 1988
) and reduce selenium concentrations
in plasma and some tissues (Bellisola et al. 1992
,
Smith and Isopenko 1997
). It is conceivable that dietary
oxidized oils, which also promote oxidative stress by reducing the
vitamin E status, could affect the selenium status of tissues and thus
interfere with the metabolism of thyroid hormones.
T4 plays a role in lipid metabolism. Hypothyroid subjects
have increased plasma concentrations of cholesterol, which are reduced
by T4 replacement (Field et al. 1986
,
Tanis et al. 1996
). In this study, there was a
significant negative correlation between the plasma concentrations of
cholesterol and T4. This suggests that the lowered
cholesterol concentrations in pigs fed the oxidized oil might have been
caused at least partially by increased plasma concentrations of
T4. T4 treatment of euthyroid rats has been
reported to increase the biliary cholesterol output (Field et al. 1986
). Rats fed an oxidized linoleic acid preparation also
exhibited increased fecal excretion of cholesterol (Hochgraf et al. 1997
). The lowered plasma cholesterol concentration in pigs
fed the oxidized oil could therefore be due to an increased excretion
of cholesterol mediated by elevated plasma thyroxine levels.
The concentrations of cholesterol in plasma and lipoproteins play an important role in the development of coronary heart disease. LDL have been considered as atherogenic lipoproteins, whereas HDL antagonize the atherogenic potential. Thus, to investigate the effects of dietary treatments on processes related to atherosclerosis, it is essential that plasma lipoproteins resemble those of humans. Because HDL are the predominant lipoprotein fraction in miniature pigs, the results are not entirely transferable to humans. A potential positive effect of reducing LDL cholesterol observed in pigs fed the oxidized oil might be neutralized by a simultaneous decrease of HDL cholesterol.
Oxidized lipoproteins play an important role in the development of
atherosclerosis, which is why the susceptibility of LDL to peroxidation
is receiving increasing attention (Steinberg et al. 1989
, Witztum and Steinberg 1991
). We used the
whole plasma oxidation assay which is considered to be an adequate
measure of lipoprotein oxidizability under the protecting influence of
water-soluble antioxidants (Kontush et al. 1997
).
The dietary oxidized oil used in this study did not increase the
susceptibility of plasma total lipids to lipid peroxidation although
tocopherol concentrations in plasma were considerably reduced by
feeding the oxidized oil. This suggests that the status of
water-soluble antioxidants was sufficiently high to protect plasma
lipids against oxidation. In terms of cholesterol concentrations and
the susceptibility of plasma lipids to peroxidation, this study
therefore provides no indication that the moderately oxidized oil
exerted proatherogenic effects. However, the development of
atherosclerosis is a complex multifactorial phenomenon which cannot be
adequately described on the basis of plasma cholesterol concentrations
and lipoprotein oxidation processes alone. There is some evidence that
highly oxidized oils accelerate the development of atherosclerosis
(Strapans et al. 1996
), and some studies report
increased concentrations of lipid peroxidation products in HDL, VLDL,
ß-VLDL and chylomicrons of rats, rabbits and humans following
ingestion of oxidized oils (Hayam et al. 1995
,
Strapans et al. 1994
, Strapans et al. 1996
). Some authors (Hochgraf et al. 1997
,
Liu and Lee 1998
) have reported that plasma cholesterol
is increased by oxidized oils, which is at variance with the results of
our study. It seems plausible that the effects of oxidized oils depend
on several experimental factors such as the amount of oil administered,
the concentrations of primary and secondary lipid peroxidation products
in the oil, the antioxidative status of the animals, the experimental
period, and others.
In conclusion, our study shows that feeding a moderately oxidized oil which does not produce general toxic effects influences the metabolism of thyroid hormones in pigs. A potential role of oxidized fats in thyroid hormone disorders should therefore be considered. Increased T4 concentrations in pigs fed the oxidized oil were associated with reduced plasma cholesterol concentrations. This study therefore indicates a close relationship between alterations of the thyroid hormone and cholesterol metabolism in pigs fed an oxidized oil. Further studies are required to understand the underlying mechanisms governing these alterations.
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FOOTNOTES |
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Manuscript received June 18, 1999. Initial review completed August 3, 1999. Revision accepted October 8, 1999.
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