We showed previously that Met deficiency at 0.25% of the diet causes elevations in plasma triiodothyronine (T3) in broilers. In the present study, plasma levels of thyroid hormones as well as insulin-like growth factors (IGF)-I and -II were measured in chicks fed 3 deficient levels of total Met. Control (0.5%) and Met-deficient diets (0.4, 0.3, and 0.2%) were fed to male broilers from 8 to 22 d of age. Additional groups of control chicks were pair-fed with the Met-deficient ones. Chicks receiving 0.4% Met increased feed intake by 10% with no significant change in body weight. The more severe Met deficiencies of 0.3 and 0.2% caused graded reductions in feed intake and weight gain. However, corresponding pair-fed control chicks were significantly heavier. These changes suggest more marked alterations in metabolic processes with 0.3 and 0.2% Met than with 0.4% Met. Liver weights were heavier in chicks fed 0.3 and 0.2% Met but not 0.4%. Plasma T3 was higher in all deficient chicks compared with the free-fed control, which was significant only with 0.3% Met. However, with 0.3 and 0.2% Met, plasma T3 was significantly elevated compared to pair-fed controls. Plasma thyroxine (T4) was lower in all deficient groups, which was significant only with 0.2% Met, whereas no significant differences occurred between deficient chicks and their pair-fed controls. Plasma IGF-I levels were not significantly different, but they were consistently lower in deficient chicks and deserve further study. Plasma IGF-II was significantly less in chicks fed 0.2% Met compared to pair-fed controls suggesting that Met deficiency interferes with IGF-II metabolism. We concluded that a deficit of dietary Met altered plasma T3 and IGF-II levels, but the effect was dependent on the degree of deficiency.
The consequences of dietary excesses of 10 essential amino acids, His, Ile, Phe, Trp, Val, Arg, Leu, Lys, Met, Thr, on growth, feed intake and plasma levels of triiodothyronine (T3) and thyroxine (T4) in growing chicks were investigated. Each amino acid was added to a starter ration to bring it to a level 2.84x above the National Research Council (1984) requirement. Excesses of all amino acids except His and Leu caused significant reductions in weight gain. Of the amino acid excesses that reduced growth, only Trp and Val did not also reduce feed intake. Gain:feed decreased significantly only in chicks consuming excess Arg, Lys, Phe, and Trp. Chicks fed excesses of Ile and Val had plasma T3 levels that were statistically higher than control levels; none of the other amino acid excesses significantly altered blood concentrations of this hormone. Compared to the control, plasma T4 levels were not significantly altered by the amino acid excesses, but there was a significant difference between Trp and Val, the latter being lower. This study shows that high dietary levels of essential amino acids cause depressions in weight gain and feed intake, and, with Ile and Val, these depressions are accompanied by elevations in plasma T3 levels. Otherwise, the amino acid excesses had little effect on plasma levels of thyroid hormones.
Consumption of low protein (10%) diets is known to produce elevations in plasma triiodothyronine (T3) in growing chickens. Therefore, we evaluated the effect of individual essential amino acid deficiencies on plasma thyroid hormone concentrations. For 13 to 15 d, chicks were fed either a control diet free-choice, one of six amino acid-deficient diets free-choice, or the control diet, pair-fed at the level consumed by chicks fed each of the deficient diets. The control diet was a 50/50 mixture of broiler starter and purified amino acid diets. The amino acids, fed at the indicated percentages of National Research Council recommendations, were: arginine, 60%; lysine, 60%; threonine, 60%; leucine, 75%; isoleucine, 75%; and methionine, 50%. Feed consumption and weight gain were significantly lower in all deficient groups than in the free-choice control group. In all cases except leucine, deficient chicks also gained less weight than their pair-fed controls. Plasma T3 levels in the groups deficient in arginine, lysine, isoleucine, or methionine were higher than in their respective pair-fed controls. However, only with the isoleucine deficiency did T3 levels exceed those of control chicks given free access to feed. Thyroxine levels were significantly lower than control levels only with the lysine deficiency. These results suggest that changes in circulating levels of thyroid hormones in a protein deficiency may be a consequence of selected amino acid deficits, because individual essential amino acids, when deficient in the diet, do not exert the same effect on circulating levels of thyroid hormones.
Adequate (1.10%) and deficient (0.88, 0.66, and 0.53%) levels of Lys were fed to broiler chicks from 9 to 23 d of age. Groups fed the control diet (1.10% Lys) were also pair-fed daily with each deficient group. Compared with the free-fed control, graded decreases in feed intake occurred as the deficiency worsened, and these were significantly different with 0.66 and 0.53% Lys. Growth decreased significantly with each deficient level of Lys compared with the free-fed control and was always significantly lower than in the pair-fed control groups in each set. Plasma triiodothyronine (T3) was elevated in chicks fed 0.88 and 0.66% lysine but not with 0.53% when compared with the full-fed control treatment. However, in deficient chicks receiving 0.66 and 0.53% Lys, T3 levels were significantly higher compared with their pair-fed controls. Plasma T4 was not significantly different between any treatments. Liver weights decreased significantly at each level of Lys deficiency, but most of the differences disappeared when expressed relative to body weight. Plasma insulin-like growth factor (IGF)-I decreased significantly with the most severe Lys deficiency. However, it decreased to a similar degree in the pair-fed controls, showing that this effect was primarily due to the lower feed intake. Plasma IGF-II levels did not differ between any treatments. No correlations were evident between thyroid hormones and IGF-I or IGF-II values. We concluded that the primary effect of Lys deficiency was an elevation in plasma T3 levels without accompanying changes in plasma T4. No effect of the Lys deficiency per se on plasma IGF-I and IGF-II and liver weights relative to body weights was found.
Broiler chicks from 2 to 4 weeks of age were fed control (0.23%) and deficient (0.115, 0.058%) levels of L-tryptophan. Separate groups of control chicks were pair-fed daily with the deficient chicks. Deficient chicks grew less efficiently than did pair-fed controls. Plasma triiodothyronine (T3) was elevated in deficient chicks, especially compared to pair-fed controls, and this was accompanied by lower reverse T3. Plasma thyroxine (T4) was also reduced with 0.059% tryptophan. However, thyroid weights and follicle diameters were unchanged. Reductions in weight gain and bone growth, increases in pituitary and pineal weights, and elevations in plasma GH occurred in the tryptophan-deficient chicks apart from any effect due to reductions in feed intake. Comb and testis size, and plasma testosterone were little affected by the deficiency. Based on changes in plasma T3 levels and feed conversion efficiencies, we conclude that tryptophan-deficient chicks show signs of relative hyperthyroidism and energy wastage compared to pair-fed controls. The elevations in plasma growth hormone and T3 support the concept that serotonin is a negative modulator of the synthesis or release of these hormones in chickens.
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