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Dietary fat type and level affect thyroid hormone plasma concentrations in rats

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The objective of the study was to examine the effect of dietary fat source and level on plasma thyroid hormone concentrations. For three weeks, male Wistar rats (n=54) were fed diets containing fats differing in fatty acid (FA) composition: sunflower oil predominantly containing polyunsaturated n-6 FA, group S; rich in monounsaturated FA rape seed oil, group R; and saturated FA palm oil, group P; at three levels (w/w): 5% LF, 10% MF, and 20% HF. Total thyroxine levels were higher in group P than R on the LF and MF diets. The free thyroxine concentration in rats on the LF diet was higher in group R than in S and P; on the MF diet, higher in group R and P than S; and on the HF diet, higher in group P than S. Triiodothyronine levels were influenced by fat composition only in rats fed the HF diet, being lower in group S than P. The results of this study suggest that diets differing with respect to fat type and level might have opposite effects on thyroid hormone values.
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3 Corresponding author: e-mail: danuta_rosolowska_huszcz@sggw.pl
Journal of Animal and Feed Sciences, 18, 2009, 541–550
Dietary fat type and level affect thyroid hormone
plasma concentrations in rats
K. Lachowicz1, I. Koszela-Piotrowska2 and D. Rosołowska-Huszcz1,3
Warsaw University of Life Sciences (SGGW),
1Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences
Nowoursynowska 159c, 02-776 Warsaw, Poland
2Nencki Institute of Experimental Biology, Department of Cellular Biochemistry
Pasteura 3, 02-093 Warsaw, Poland
(Received 10 June 2008; revised version 26 March 2009; accepted 24 June 2009)
ABSTRACT
The objective of the study was to examine the effect of dietary fat source and level on plasma
thyroid hormone concentrations. For three weeks, male Wistar rats (n=54) were fed diets containing
fats differing in fatty acid (FA) composition: sunower oil predominantly containing polyunsaturated
n-6 FA, group S; rich in monounsaturated FA rape seed oil, group R; and saturated FA palm oil,
group P; at three levels (w/w): 5% LF, 10% MF, and 20% HF. Total thyroxine levels were higher in
group P than R on the LF and MF diets. The free thyroxine concentration in rats on the LF diet was
higher in group R than in S and P; on the MF diet, higher in group R and P than S; and on the HF diet,
higher in group P than S. Triiodothyronine levels were inuenced by fat composition only in rats fed
the HF diet, being lower in group S than P. The results of this study suggest that diets differing with
respect to fat type and level might have opposite effects on thyroid hormone values.
KEY WORDS:
thyroid, thyroxine, triiodothyronine, reverse-triiodothyronine, nutrition, fatty acids,
rats
INTRODUCTION
Thyroid hormones (TH) are involved in the regulation of both anabolic and
catabolic pathways of protein (Rooyackers and Sreekumaran, 1997; Clément
et al., 2002), lipid (Yen, 2001) and carbohydrate (Feng et al., 2000) metabolism.
The main hormone secreted by the thyroid, 3,3’,5,5’tetraiodothyronine (thyroxine,
542 FAT TYPE – THYROID HORMONE IN RAT PLASMA
T4), undergoes deiodination in target tissues, either in the outer ring leading to
metabolically active 3,3’,5 triodothyronine (T3), or in the inner ring, giving inactive
3,3’,5’ reverse T3 (rT3) (Köhrle, 2007). The metabolic effects of the TH result from
the binding of T3 to specic nuclear receptors (THR) (Oetting and Yen, 2007).
Excess or deciency of TH leads to malfunctioning of the cardiovascular (Biondi
and Klein, 2004), nervous (Ahmed et al., 2008) and endocrine (Mastorakos et al.,
2007) systems, white and brown adipose tissues (Yen, 2001), or bones (Lakatos,
2003), and in consequence, to the impairment of homeostasis manifesting as obesity
(Krotkiewski, 2002), metabolic syndrome (Lin et al., 2005), diabetes (Alrefai et al.,
2002) and/or atherosclerosis (Biondi and Klein, 2004).
Nutrition, both the amount and composition of food, level of macronutrients and
specic micronutrients, has been shown to affect hypothalamo-pituitary-thyroidal
axis activity (Kopp, 2004). Dietary fatty acid composition has been found to
inuence thyrotropin (TSH) secretion (Clandinin et al., 1998), thyroid peroxidase
(TPO) (Lachowicz et al., 2008), hepatic type I deiodinase (DI) activities (Kahl et
al., 1998; Lachowicz et al., 2008), and T3 binding to nuclear receptors (Yamamoto
et al., 2001). The combined effect of dietary fat level and composition on thyroid
hormone plasma concentrations are not yet sufciently characterized despite
their importance to dietary practice. Thus, the aim of this work was to determine
the response of TH plasma concentrations to dietary fats differing in fatty acid
composition and given in low, moderate or high amounts.
MATERIAL AND METHODS
Experimental design
The experiment was conducted on 54 male Wistar rats weighing 277 g (SEM
4.23 g) at the start of the experiment. The animals were housed individually
under stable environmental conditions (illumination, 12 light: 12 dark cycle;
temperature, 23oC; air humidity, 50-65%) with free access to feed and water.
After a two-week adaptation period, the animals were divided into 9 groups (n=6)
and fed on diets differing in fat content (w/w): 5%, low fat (LF), 10%, medium fat
(MF), 20%, high fat (HF) and fat source: sunower oil (predominantly containing
n-6 18:2 linoleic acid, group S), rape seed oil (rich in 18:1 monounsaturated oleic
acid, group R), and palm oil (rich in saturated palmitic acid, group P) for three
weeks. Diet compositions are given in Table 1, the fatty acid content of dietary
fats, in Table 2.
At the end of the experiment the rats were sacriced and blood was collected
by cardiac puncture. Plasma was stored at -23oC for hormone determination.
543LACHOWICZ K. ET AL.
The study protocol was approved by the Local Animal Care and Use Committee
in Warsaw.
Table 1. Composition of experimental diets (Gronowska-Senger and Pierzynowska, 2002), g per
100 g
Item Low fat, LF Medium fat, MF High fat, HF
Components
wheat starch 68 63 53
casein 18 18 18
fat15 10 20
potato starch 5 5 5
vitamin mixture2111
mineral mixture3333
choline chloride 0.2 0.2 0.2
gross energy, MJ per 100 g diet 1.50 1.61 1.82
Energy supplied, %
fat
carbohydrates
protein
11.8 22.8 38.5
70.8 61.1 46.7
17.5 16.1 14.8
1 sunower S, rape seed R and palm P oils were used; 2 vitamin mixture composition per 100 g
of mixture; IU: vit. A 200 000, vit. D3 20 000, vit. E 1000; mg: vit. K 50; riboavin 80, thiamin
chloride 50, pyridoxine chloride 50, biotin 4, vit. B12 0.3; g: PABA 1, inosytol 1, niacin 0.4, calcium
pantothenate 0.4; 3 mineral mixture composition per 100 g of mixture, g: CaHPO4 73.5, K2HPO4
8.1, K2SO4 6.8, NaCl 3.06, CaCO3 2.1, Na2HPO4 2.14, MgO 2.5; mg: C3H4(OH)(COO)2 Fe 558,
ZnCO3 81, MnCO3 421, CuCO3 33, C3H4(OH)(COOH)3, 706; µg: KJ 720
Table 2. Content of fatty acids and total saturated fatty acids (SFA), monounsaturated fatty acids
(MUFA) and polyunsaturated fatty acids (PUFA) in dietary fats, g per 100 g fat
Fatty acids Sunower oil Rape seed oil Palm oil
C16:0 6.03 5.44 47.24
C18:0 3.40 1.19 2.65
∑SFA 10.50 6.63 51.89
C16:1 0.04 0.00 2.77
C18:1 n-9 22.18 62.31 36.08
∑MUFA 23.02 62.85 43.31
C18:2 n-6 65.91 25.16 4.07
C18:3 n-3 0.40 5.36 0.00
∑PUFA 66.31 30.52 4.07
Chemical analysis
Plasma concentrations of thyroxine, both total and free (T4 and fT4),
triiodothyronine (T3), and reverse T3 (rT3) were determined by radioimmuno-
assay using commercial kits. For T4 (sensitivity 12.8 nmol/l, intraassay
variation 5.3%, interassay variation 4.1%) and T3 (sensitivity 0.154 nmol/l,
intraassay variation 3.8%, interassay variation 5.4%) the kits used were
544 FAT TYPE – THYROID HORMONE IN RAT PLASMA
from POLATOM; for fT4 (sensitivity 0.8 pmol/l, intraassay variation 5%,
interassay variation 7%) the kit was from Orion Diagnostica, and for rT3 (sensi-
tivity 0.014 nmol/l, intraassay variation 6.5%, interassay variation 7.6%) the
kit was from Biochem Immunosystems.
Statistical analysis
Statistical analysis (two-way variance ANOVA and simple regression) was
performed using Statistica 6.0 software. Signicant differences between groups
were determined by post hoc derivation of the least signicant difference between
means (LSD) at the level of P0.05. All data are expressed as means±SEM.
RESULTS
Body weight gain, feed energy efciency and fatty acid intake, as well as
free fatty acid: palmitic (C16:0), stearic (C18:0), oleic (C18:1), linoleic (C18:2),
linolenic (C18:3), arachidonic (C20:4) and docosahexanoic (C22:6), triacylo-
glicerol and cholesterol concentrations in the plasma are presented in Tables 3-5.
Table 3. Body weight gain (BWG), feed intake (FI) and efciency of energy (FE). Values expressed
as the mean with standard error for six animals
Variables Diets1
Dietary groups2
S R P
mean SEM mean SEM mean SEM
BWG
g/day
LF 3.69aB 0.21 3.03a 0.21 2.71A 0.31
MF 3.72a0.27 3.44 0.16 3.00 0.30
HF 4.98bB 0.45 3.90bA 0.29 3.36A 0.14
FI
g/day
LF 22.52 0.40 21.79 0.46 22.94 0.50
MF 22.90 0.52 20.89 0.66 22.23 0.82
HF 21.84 0.69 21.45 0.59 20.35 0.83
FE
g BWG/1kJ
LF 10.98B0.46 9.01A0.51 7.85A 0.81
MF 9.99a0.53 10.23B0.78 8.38A 0.74
HF 12.62bB 1.12 9.94A 0.31 9.14A0.49
different a,b,c letters indicate signicant differences within groups S, R or P (P0.05)
different A,B,C letters indicate signicant differences between groups S, R and P (P0.05)
1,2 explanation see Table 1
545LACHOWICZ K. ET AL.
Table 4. Intake of fatty acids, mg per day per 100 g of nal body weight
Fatty acids Diets1
Dietary groups2
S R P
mean SEM mean SEM mean SEM
C16:0
LF 18.1aA 0.3 15.5aA 0.2 158.9aB 4.0
MF 39.2aA 0.1 31.7aA 1.0 296.7bB 10.0
HF 64.6bA 2.4 60.0bA 1.7 498.2cB 19.4
C18:0
LF 10.2aB 0.2 3.4aA 0.0 8.9aB 0.2
MF 22.1bC 0.2 6.9bA 0.2 16.6bB 0.6
HF 36.4cC 1.3 13.1cA 0.4 27.9cB 10.9
C18:1
LF 66.4aA 1.0 177.3aC 2.2 121.4aB 3.0
MF 144.0bA 1.3 362.6bC 11.1 226.6bB 7.7
HF 237.6cA 8.7 687.0cC 19.4 380.5cB 148.2
C18:2
LF 197.5aC 3.0 71.6aB 0.9 13.7aA 0.3
MF 428.0bC 4.0 146.4bB 4.5 25.6A 0.9
HF 706.2cC 25.9 277.4cB 7.9 42.9bA 1.7
C18:3
LF 1.20aA 0.02 15.25aB 0.19 0.00 0.00
MF 2.60A 0.02 31.19bB 0.96 0.00 0.00
HF 4.29bA 0.16 59.10cB 1.67 0.00 0.00
1,2 explanation see Table 1
Thyroxine. The total thyroxine concentration (Figure 1A) was signicantly
affected by dietary fat composition (ANOVA; P<0.002). However, this effect
was seen only in rats consuming LF and MF diets, where T4 levels were higher
in group P than S and R in animals on the LF diet and higher in group P than R in
rats on the MF diet. An effect of fat level on plasma T4 concentration was observed
only in groups S and R. In group S, the T4 concentration was higher in animals on
the MF diet than in those on diets LF and HF, which did not differ signicantly.
In group R, T4 was higher in rats fed the HF diet than in the group receiving LF
diets.
The plasma free T4 concentration (Figure 1B) was inuenced by fat composition
relative to its level (ANOVA, effect of fat composition, P<0.0001; effect of
interaction between fat level and composition, P<0.0004); in rats fed the LF diet
it was signicantly higher in group R than in S and P. Among rats receiving the
MF diet, fT4 was higher in groups R and P than in S, whereas in rats fed the HF
diet, it was higher in group P than S. In group P, fT4 was lower in rats fed LF
compared with diets MF and HF. In group R, the fT4 concentration fell as the fat
level rose, being lowest in rats receiving the HF diet. In group S, the effect of fat
level did not occur. The free T4 concentration was directly related to the levels of
plasma cholesterol (r=0.41, P<0.01), C18:1 (r=0.44, P<0.04), and C20:4 (r=0.67,
P<0.0001).
546 FAT TYPE – THYROID HORMONE IN RAT PLASMA
Table 5. Plasma FA, TAG and cholesterol concentrations
Variables Diets1
Dietary groups2
S R P
mean SEM mean SEM mean SEM
C16:0
µmol/l
LF 179.75b 35.21 140.60 34.56 140.00a 31.77
MF 161.67b 24.83 109.50 10.93 153.40a 36.09
HF 73.25aA 14.82 113.75A 6.00 268.60bB 56.61
C18:0
µmol/l
LF 130.75bB 19.35 47.20A 14.55 50.80aA 15.59
MF 134.50bB 21.42 46.83A 10.56 56.00A 9.91
HF 27.25aA 4.62 44.25A 13.11 96.40bB 17.58
C18:1
µmol/l
LF 77.75 33.19 94.25 64.67 165.60a 54.66
MF 87.67 18.49 202.50 49.76 243.33 84.01
HF 74.67A 22.28 208.00 35.34 338.33bB 118.64
C18:2
µmol/l
LF 157.50 43.79 144.33 38.09 103.20 46.67
MF 214.50 38.55 173.67 46.77 84.20 28.60
HF 171.00 70.00 205.25 40.64 182.00 61.80
C18:3
µmol/l
LF 6.25 0.75 11.17a 3.19 6.00 3.11
MF 7.33A 3.32 17.33bB 4.61 1.80A 0.37
HF 2.33A 0.88 21.00cB 4.18 5.40A 2.25
C20:4
µmol/l
LF 39.67 10.52 74.83 19.60 49.40 12.64
MF 44.17 6.59 46.83 7.80 54.20 13.37
HF 30.00 6.64 40.50A 7.42 70.60 16.00
C22:6
µmol/l
LF 32.00 2.08 21.00A 5.14 14.20 2.80
MF 22.67 2.82 17.50 1.84 15.40 2.23
HF 6.50 0.64 16.75B 1.25 22.20 2.27
Tg
µmol/l
LF 1.26 0.11 1.52 0.16 1.27 0.16
MF 1.02 0.08 1.56 0.34 1.34 0.24
HF 1.14 0.15 1.27A 0.09 1.78 0.23
Cholesterol
mg/dl
LF 58.08 3.82 77.36 4.46 65.68 5.13
MF 57.73 3.09 61.50 8.82 63.48 8.77
Triiodothyronine. The plasma concentration of triiodothyronine (Figure 2A)
was not signicantly altered by dietary fat composition among rats fed the LF and
MF diets, but in rats receiving the HF diet the T3 level was signicantly lower in
group S than in P. The fat level signicantly inuenced plasma T3 concentrations
only in group S, in which the hormone level was lower in animals on the HF diet
than in those on diets MF and LF. Triiodothyronine levels were directly related
to plasma C18:1 (r=0.38, P<0.03), C18:2 (r=0.42, P<0.006) and C20:4 (r=0.57,
P<0.001) concentrations.
547LACHOWICZ K. ET AL.
Figure 1. Plasma total thyroxine (T4 [nmol/l] - panel A), free thyroxine (fT4 [pmol/l] - panel B)
concentrations in rats fed diets containing 5% (LF), 10% (MF) or 20% (HF) (w/w) sunower oil
(group S), rape seed oil (group R) or palm oil (group P) for three weeks. Values are expressed as the
mean with standard error for six animals; different a, b letters indicate signicant differences within
groups S, R and P (P0.05); different A, B letters indicate signicant differences between groups
S, R and P (P0.01)
Figure 2. Plasma triiodothyronine (T3 [nmol/l] - panel A) and reverse triiodothyronine (rT3 [nmol/l]
- panel B) concentrations. Explanations see Figure 1
Reverse-triiodothyronine. According to ANOVA, the plasma concentration
of reverse T3 (Figure 2B) was not signicantly affected by either fat level or
composition. However, in group R, the rT3 level was higher in animals on the HF
diet than in those on the MF diet, and these values were higher than in group S fed
the HF diet. The reverse T3 level was directly related to C18:1 (r=0.38, P<0.001),
and C18:3 (r=0.51, P<0.005) intakes.
DISCUSSION
Plasma concentrations of T3, reverse T3, T4 and fT4 responded to dietary fat level
and composition in various ways. The triiodothyronine concentration was affected
Groups
Groups
fT4, pmol/l
110
88
66
44
22
0
0
28
56
84
112
140
S
R
P
P
R
S
LF
MF
HF
HF
MF
LF
A
B
aA
b
a
aA
A
b
B
B
A
A
A
cB
bB
a
aA
bB
bB
Groups
Groups
T3, nmol/l
rT3, nmol/l
0.14
0.11
0.08
0.06
0.03
0.00
0.00
0.30
0.60
0.90
1.20
1.50
S
R
P
P
R
S
LF
MF
HF
HF
MF
LF
A
B
b
b
aA
B
A
bB
a
548 FAT TYPE – THYROID HORMONE IN RAT PLASMA
by fat level only in rats fed sunower (S) oil. This nding partly corroborates the
results of studies reporting a decrease in T3 concentration caused by high fat diets
(Otten et al., 1980; Vermaak et al., 1986). However, it is difcult to explain the lack
of effect of fat level on the T3 concentration in rats fed palm (P) and rape seed (R)
oils. Rats in group S consumed the highest amounts of n-6 PUFA. In contrast to
our results, a high fat diet rich in n-6 PUFA has previously been found to increase
plasma levels of T3 and T4 compared with a high fat diet rich in n-3 PUFA and
a high carbohydrate diet (Tsuboyama-Kasaoka et al., 1999). On the other hand,
higher levels of T3 and T4 have been found in rats receiving n-3 and n-6 PUFA
fatty acids compared with those fed saturated fatty acids (Takeuchi et al., 1995).
Reverse T3 is considered to reect, to the same degree, in a reciprocal manner,
hepatic deiodinase type I activity (Danforth i Burger, 1989). Our investigations
could conrm such relations since in the present study, rT3 was directly related to
C18:1, C18:2 and C20:4 acid intakes, whereas under the same conditions, hepatic
DI activity was negatively correlated with C18:1 and C18:2 intakes (Lachowicz
et al., 2008).
An effect of fat amount on plasma T4 concentrations was seen in groups S
and R. However, in line with other reports (Otten et al., 1980; Vermaak et al.,
1986), only in rats fed sunower oil did the HF diet induce lower T4 levels than in
animals consuming the MF diet. The different relationship between plasma levels
of fatty acids with T3 concentration and with DI activity (Lachowicz et al., 2008)
suggest that factors other than hepatic DI inuenced the T3 variability seen in this
study. Plasma concentrations of triiodothyronine and free T4, but not total T4, were
similarly related to plasma lipid metabolism indices. Their correlations with the
triglyceride concentration were the opposite of those observed with TPO activity
(Lachowicz et al., 2008). The direct relationship between free T4 levels and plasma
concentrations of oleic, arachidonic and linoleic acid found here may be explained
by competition between T4 and arachidonic acid in binding to transthyretin and
thyroid hormone binding globulin, which are also found in humans (Lim et al.,
1995).
The results reect the complexity of the effects of fatty acids on plasma thyroid
hormone levels. It seems that MUFA intake with rape seed oil might have induced
lower T4 and higher fT4, with no effect on T3 concentration compared with the
palm oil-fed groups. In contrast to this, high-fat diets rich in n-6 PUFA might
have had a similar effect on T3 and T4 levels. Unsaturated fatty acids could have
altered the thyroid hormone plasma prole secondary to their impact on peripheral
enzyme pathways, as well as by competing with thyroid hormones in binding to
plasma proteins.
549LACHOWICZ K. ET AL.
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... On the other hand, T 4 and T 3 :T 4 ratio were not affected by dietary fat sources. Thyroid hormones decreased during hot weather and are involved in the regulation of anabolic and catabolic pathways of protein, lipid and carbohydrate metabolism (68,69). A previous study reported that a significant interaction between the type and level of fats might have adverse effects on T 3 and T 4 levels (68,69). ...
... Thyroid hormones decreased during hot weather and are involved in the regulation of anabolic and catabolic pathways of protein, lipid and carbohydrate metabolism (68,69). A previous study reported that a significant interaction between the type and level of fats might have adverse effects on T 3 and T 4 levels (68,69). The dietary fatty acid profile reportedly affects deiodinase hepatic type I activity (68,69) and binding of T 3 to nuclear receptors (70). ...
... A previous study reported that a significant interaction between the type and level of fats might have adverse effects on T 3 and T 4 levels (68,69). The dietary fatty acid profile reportedly affects deiodinase hepatic type I activity (68,69) and binding of T 3 to nuclear receptors (70). This finding partially contradicts the results of research that showed a reduction in T 3 level of animals fed high-fat diets (71,72). ...
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This research evaluate the influence of different oil sources, namely fish oil (FO), coconut oil (CocO), canola oil (CanO), or a mixture of the three oils (MTO)—included at 1.5% in broiler diets—compared to a no oil-supplemented diet. Hence, 250 unsexed, 1-day-old Cobb chicks were weighed and randomly allocated into five dietary treatment groups of 50 chicks each and five replicates per group. Oil-supplemented diets significantly increased the growth, improved the feed conversion ratio (FCR), and decreased the abdominal fat percentage compared to the control diet. Amylase was significantly elevated due to feeding the FO- or CocO-supplemented-diet compared to the control diet, whereas lipase increased due to offering CocO- and CanO-enriched diet; chymotrypsin increased due to different oil sources. High-density lipoprotein cholesterol (HDL-C) increased markedly due to offering an oil-supplemented diet, but low-density lipoprotein cholesterol (LDL-C), the LDL-C:HDL-C ratio, and malondialdehyde (MDA) decreased. Blood plasma immunoglobulin (Ig) G and IgM significantly increased due to feeding CocO, CanO, or MTO compared to the control group, whereas FO increased IgG only. FO- and CanO-containing diets resulted in the highest increase in α2-globulin and γ-globulin. The antibody titer to avian influenza (HIAI) and Newcastle disease (HIND) were significantly elevated due to CocO supplementation compared to the control group. The bursa follicle length and width and thymus cortex depth were increased considerably due to the FO-supplemented diet compared to the control, but the follicle length:width ratio decreased. The villus height:depth ratio was significantly elevated due to both the CanO and MTO diets. The antioxidant status improved considerably due to the addition of CocO and CanO. Both CanO and MTO similarly increased plasma T3, T4, and the T3:T4 ratio. In conclusion, oil supplementations at 1.5% enhanced growth performance and immune status, improved the blood lipid profile and antioxidants status, and the effect of the oil sources depends on the criteria of response.
... Chickens received linseed and corn oils had the highest levels of T3 and T4 and those fed palm and olive oils had the lowest levels (p < 0.05). An interesting study showed that lipid source and level may have opposite effects on thyroid hormone levels (Lachowicz, Koszela-Piotrowska, & Rosołowska-Huszcz, 2009). The increase in T3 and T4 levels related to the effects of fatty acids on thyrotropin secretion (Clandinin, Claerhout, & Lien, 1998). ...
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The research aimed to elaborate the influence of designed mixtures used in broilers fattening on the concentration of electrolytes and thyroid gland hormones in the blood. The research was carried out on 120 male Ross 308 hybrid broilers. The fattening lasted for 42 days. During the first three weeks of fattening broilers were fed standard starter diet containing 22% crude protein and 13.90 MJ/kg ME. During the last three weeks of fattening, broilers were divided into 6 experimental groups, each fed specially prepared finisher diets (P1=6% sunflower oil+0.0 mg Se/kg of feed, P2=6% linseed oil+0.0 mg Se/kg of feed, P3=6% sunflower oil+0.3 mg Se/kg of feed, P4=6% linseed oil+0.3 mg Se/kg of feed, P5=6% sunflower oil+0.5 mg Se/kg of feed, P6=6% linseed oil+0.5 mg Se/kg of feed). Finisher diet was balanced at 18.02% crude protein and 14.40 MJ/kg ME. It was found out that the type of oil in chicken feed influenced to blood pH (P <0.001), whereas selenium level (P=0.014) in the feed, as well as the oil type and selenium level interaction (P<0.001) influenced the concentration of potassium in the blood. Oil type (P=0.037) influenced the concentration of fT3, which was lower in chickens fed mixtures with addition of linseed oil than in the chickens fed sunflower oil added mixtures. Interaction of selenium content and oil type had influence on differences in concentration of fT4 as well as on the ratio of fT3/fT4, (P<0.001, i.e. P=0.021). The research results indicated that oils supplemented to broiler diets and combined with different organic selenium concentrations affected pH, concentration of some electrolytes and thyroid gland hormones in broiler blood, however, all obtained values were within reference range for poultry.
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The effect of dietary fat level and composition on the activities of enzymes involved in thyroid hormone metabolism: thyroid peroxidase (TPO) and hepatic type I deiodinase (DI) were investi- gated. Male Wistar rats weighing on average 277 g (SEM=4.23 g) received different levels (w/w 5%-LF, 10%-MF, 20%-HF) and types of dietary fat (sunfl ower oil - group S, rape seed oil - R and palm oil - P) over a three weeks. TPO rose with fat intake in group R and declined in groups S and P. Hepatic DI activity was not affected by dietary fat composition, but was infl uenced by fat level, decreasing as fat intake increased. The infl uences of dietary fat level and composition on thyroid physiology are interdependent. TPO and DI activity seem to respond in a differentiated manner to changes in the amount and type of fatty acids consumed.
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The conversion of thyroxine (T4) to the metabolically active thyroid hormone, triiodothyronine (T3), is catalyzed by iodothyronine 5′-monodeiodinase (EC 3.8.1.4; 5′D). Indian River male broiler chickens growing from 7 to 28 d of age were used in a 3 × 2 factorial to determine the effect of dietary energy from fat and T3 supplementation on hepatic 5′D activity and plasma concentration of T4 and T3. Chickens were fed diets (13.1 MJ/kg diet) containing 1.25 (LF), 2.5 (MF) and 5.00 (HF) MJ from fat/kg diet + 0 or 1 mg T3/kg diet. Blood and liver samples were collected on d 28. Hepatic 5′D was affected by fat × T3 interaction (P<0.01): with no added T3, MF and HF increased 5′D 25 (P<0.01) and 16% (P<0.05) as compared to LF (1.5 nmoles I- · hr−1 · mg protein−1); however no changes in 5′D were found when T3 was added (1.42, 1.35 and 1.36 for LF, MF and HF, respectively). Diets with T3 increased plasma T3 (5.1 vs. 18.1 nmol/L, P<0.001) and decreased plasma T4 (12.4 vs. 7.9 nmol/L, P<0.001). Dietary fat did not affect plasma T3 and T4. The data indicate that the hepatic generation of T3 is stimulated by increased dietary fat intake. This effect of fat, however, is inhibited by dietary T3 supplementation.
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The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.
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Short term changes in serum 3,3',5-triiodothyronine (T3) and 3,3'5-triiodothyronine (reverse T3, rT3) were studied in four healthy nonobese male subjects under varying but isocaloric and weight maintaining conditions. The four 1500 kcal diets tested during 72 hr, consisted of: I, 100% fat; II, 50% fat, 50% protein; III, 50% fat, 50% carbohydrate (CHO), and IV, a mixed control diet. The decrease of T3 (50%) and increase of rT3 (123%) in the all-fat diet equalled changes noted in total starvation. In diet III (750 kcal fat, 750 kcal CHO) serum T3 decreased 24% (NS) and serum rT3 rose significantly 34% (p < 0.01). This change occurred in spite of the 750 kcal CHO. This amount of CHO by itself does not introduce changes in thyroid hormone levels and completely restores in refeeding models the alterations of T3 and rT3 after total starvation. The conclusion is drawn that under isocaloric conditions in man fat in high concentration itself may play an active role in inducing changes in peripheral thyroid hormone metabolism.
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The hydrolysis of lecithin by phospholipase produces equimolar amounts of nonesterified fatty acids (NEFAs) and lysolecithin. In this study, we have evaluated the effect of lysolecithins and NEFAs on thyroid hormone binding by examining their interactions with thyroxine-binding globulin (TBG)(serum 1:10,000 dilution) and purified transthyretin (TTR). Unsaturated NEFAs (palmitoleic, oleic, linolenic, arachidonic, eicosapentaenoic, and docosahexaenoic acid) inhibited [125I]T4 binding to TBG. Their affinities, relative to unlabeled T4, ranged from 0.005 to 0.0016%, except for oleic acid with relative affinity of < 0.0005%. Saturated NEFAs, lauric, myristic, palmitic, and stearic acid were inactive. After purification by high-performance liquid chromatography, 1-oleoyl and 2-oleoyl lysolecithin displaced [125I]T4 from TBG with an affinity of 0.0006 and 0.0005%, respectively. On a molar basis, this affinity was approximately 10-fold lower than arachidonic acid, the most potent NEFA in inhibiting T4 binding to TBG in this assay system. Of all the NEFAs tested, only arachidonic acid inhibited [125I]T4 binding to TTR, with an affinity relative to unlabeled T4 of 0.49%. 1-Oleoyl, 1-palmitoyl, and 1-stearoyl lysolecithin were without effect on TTR binding. The T4-displacing effects of NEFAs are markedly attenuated by their extensive binding to albumin. Using purified [14C]NEFA preparations and heptane partitioning, the mean unbound percentages of linoleic, eicosapentaenoic, and docosahexaenoic acid in undiluted normal human serum were 0.00099, 0.0050, and 0.0042%, respectively (n = 3). In view of the very high degree of albumin binding of NEFAs, studies in diluted serum will grossly overestimate their competitor potency. The affinities of lysolecithins for the T4 binding sites of TBG and TTR are lower than those of NEFAs and depend on the fatty acid component. Lysolecithins are unlikely to influence plasma protein binding of T4 during critical illness.
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It has been shown previously that dietary fat type influences body fat accumulation in rats. The effects of dietary fat type on serum thyroid hormone, activity of Na+,K(+)-ATPase and lipoprotein lipase were studied. Rats were fed an experimental diet containing lard, high oleic safflower oil, safflower oil or linseed oil for 12 wk. Carcass fat content was significantly higher in rats fed the lard diet than in those fed the other diets. However, intra-abdominal adipose tissue weights were not affected by type of dietary fat. The serum triiodothyronine concentration and the activity of Na+,K(+)-ATPase in the liver and skeletal muscle were significantly lower in the lard diet group than in the other diet groups. The lipoprotein lipase activity of abdominal subcutaneous fat was significantly higher in rats fed the lard diet than in rats fed the other diets, but the activity of lipoprotein lipase in intra-abdominal fat was not significantly different. These results suggest that the intake of lard, compared with the intake of the vegetable oils, may decrease Na+,K(+)-ATPase activity in the liver and skeletal muscle by lowering serum triiodothyronine concentration, resulting in the promotion of body fat accumulation.
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A continuous turnover of protein (synthesis and breakdown) maintains the functional integrity and quality of skeletal muscle. Hormones are important regulators of this remodeling process. Anabolic hormones stimulate human muscle growth mainly by increasing protein synthesis (growth hormone, insulin-like growth factors, and testosterone) or by decreasing protein breakdown (insulin). Unlike in growing animals, insulin's main anabolic effect on muscle protein in adult humans is an inhibition of protein breakdown. Protein synthesis is stimulated only in the presence of a high amino acid supply. A combination of the stress hormones (glucagon, glucocorticoids, and catecholamines) cause muscle catabolism, but the effects of the individual hormones on human muscle and their mechanisms of action remain to be clearly defined. Although thyroid hormone is essential during growth, both an excess and a deficiency cause muscle wasting by yet unknown mechanisms. A greater understanding of the regulation of human muscle protein metabolism is essential to elucidate mechanisms of muscle wasting.
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Circulating levels of thyroid-stimulating hormone (TSH), growth hormone (GH), adrenal corticotrophic hormone (ACTH) and prolactin (PRL) were assessed in suckling rats in the postweaning period after rats were fed diets that reflect the fat composition of a current infant formula with or without the addition of 1.2 g/100 g fatty acid arachidonic acid [20:4(n-6)] and 0.7 g/100 g fatty acid docosahexaenoic acid [22:6(n-3)] or both 20:4(n-6) and 22:6(n-3). At 2 wk of age, no effect of diet on circulating levels of TSH, ACTH, GH or PRL was apparent. By 6 wk of age (3 wk postweaning), male rats consuming the diet containing 22:6(n-3) had significantly elevated levels of TSH, and females had significantly higher ACTH concentrations than males. No effect of diet was observed on circulating GH or PRL levels. Male pups had higher levels of TSH than females (P < 0.0001), whereas female pups from the 22:6(n-3) diet treatment exhibited much higher levels of ACTH than all male pups from any of the other diet treatments. These results suggest that metabolic controls, functioning through endocrine mechanisms, can be altered by changing the 20:4(n-6) to 22:6(n-3) balance in the diet.