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F A Alster

Publications and source records attributed to F A Alster.

10 recordsLinked to original sources
PubMed2003

Effects of methionine deficiencies on plasma levels of thyroid hormones, insulin-like growth factors-I and -II, liver and body weights, and feed intake in growing chickens.

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.

Animals↗
PubMed1998

Growth, feed intake, and plasma thyroid hormone levels in chicks fed dietary excesses of essential amino acids.

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.

Amino Acids, Essential↗
PubMed1997

Growth and plasma thyroid hormone concentrations of chicks fed diets deficient in essential amino acids.

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.

Amino Acids, Essential↗
PubMed1997

Dietary carbohydrate and fat do not alter the thyroid response to protein deficiency in chicks.

Consumption of low-protein diets consistently causes elevations in circulating levels of triiodothyronine (T3) in several species of animals. In chicks this is often accompanied by lower levels of circulating thyroxine (T4). Since low-protein diets are usually formulated by replacing the detected protein with carbohydrate, the question arises as to whether the changes in thyroid hormones are a result of the lower protein or higher amounts of carbohydrate in such diets. Male broiler chicks, 13-26 days of age, were fed experimental diets that contained either an adequate level of protein (24%) or levels that were slightly (17%) or moderately (10%) deficient in protein. The deleted protein was replaced, isocalorically, with either glucose, soybean oil, or hydrogenated coconut fat. Though the level of protein and source of energy differed among diets, all diets contained identical amounts of all nutrients and energy, and were of similar weight densities. Circulating levels of thyroid hormones were measured from blood samples taken at the end of the study. Plasma T3 was elevated to a similar degree in all protein-deficient animals compared with control. Plasma T4 decreased in all protein-deficient chicks and was lowest with 10% dietary protein. Changes in circulating levels of thyroid hormones occurred independently of the source of dietary energy. Therefore, it is concluded that alterations in circulating levels of thyroid hormones that occur in chicks fed low-protein diets are a specific effect of the protein deficit and are not a related to the amounts of carbohydrate or fat present in the diet.

Animals↗
PubMed1992

Growth, thyroid function, and serum macromineral levels in magnesium-deficient chicks.

Growth and thyroid function were studied in Mg-deficient chicks. Dietary levels of 80 to 315 ppm Mg were compared with control levels of 578 to 787 ppm Mg. Signs of Mg deficiency appeared rapidly and acutely within 2 to 5 days at dietary levels of 250 to 260 ppm or lower. Growth and feed intake decreased progressively as the deficiency became more severe. Control chicks pair-fed with the deficient chicks gained significantly more weight. Serum Mg decreased at all levels of Mg below control, but at 260 and 315 ppm it returned to control values after 21 days on treatment. Serum Ca diminished only when dietary Mg was 250 ppm or less. Serum K increased in severely deficient chicks but decreased over time in milder deficiencies. Thyroid gland weights were unchanged. However, very young chicks fed a Mg-deficient diet had lower serum 3,5,3'-triiodothyronine (T3) whereas serum thyroxine (T4) was generally unaffected. Beyond 1 wk of age chicks that had prior access to a Mg-sufficient diet had low serum T4 levels whereas serum T3 was unchanged. Therefore, peripheral thyroid hormone metabolism is altered in a Mg deficiency, but this effect is dependent on the age at which the deficiency occurs.

Animals↗
PubMed1987

Thyroid function, energy balance, body composition and organ growth in protein-deficient chicks.

Protein-deficient diets (17, 10, 6.5 or 3% protein) and a 24% control diet were fed to growing chicks. A control group was pair-fed daily with each deficient group. Energy intake was lower in the 6.5 and 3% protein groups than in the other groups. However, weight gain, bone growth and feed conversion efficiency were lower with 10% protein or less. Relative thyroid weights were unaffected by dietary protein. Plasma T3 (3,5,3'-triiodothyronine) levels were significantly higher in all deficient groups, whereas plasma T4 (thyroxine) was lower. Plasma rT3 (reverse T3) was unaffected by the protein deficiencies, suggesting that enhanced conversion of T4 to T3 rather than to rT3 had occurred. Hepatic alpha-glycerol-3-phosphate dehydrogenase (alpha-GP) shuttle activity increased markedly in protein-deficient chicks. Efficiency of energy utilization was unaltered in chicks fed 17 or 10% protein but was higher in chicks fed 6.5 and 3% protein than in controls. All deficient chicks had more fat and less protein and water in the tissues. The lower feed conversion efficiency therefore represents almost entirely a shift in body composition toward fat and does not reflect a loss of energy as heat. We conclude that elevations in plasma T3 and in thyroid-controlled alpha-GP shuttle activity, although sensitive indicators of protein deficiencies, are not good predictors of altered thermogenic activity in protein-deficient chicks.

Animals↗
PubMed1987

Thyroid function, growth hormone, and organ growth in broilers deficient in phosphorus.

The effects of a dietary P deficiency on thyroid function, serum growth hormone, and growth parameters in 10 to 29-day-old broiler cockerels was determined. Chicks fed severely P-deficient diets (.05% or .10% available P) grew more slowly and ate less feed than controls fed .65% P. The deficiency was also accompanied by hypercalcemia, hypophosphatemia, and decreases in percent bone ash, fat-free tibial weight, and tibial length and width. Increases in the relative weights of kidneys, hearts, and pituitary glands (.05% P only) occurred as well. Most of these changes occurred to a lesser extent or not at all in pair-fed controls, showing that they resulted specifically from the P deficiency and were not simply a result of reductions in feed intake. Phosphorus deficiency also was accompanied by peripheral edema and hydropericardium. Relative thyroid weight was unaffected. Serum triiodothyronine was consistently lower in the P-deficient chicks, although effects were significant only in one experiment. Thyroxine levels tended to be low also, but not consistently so. Serum growth hormone in P-deficient chicks in both studies was consistently lower than that in pair-fed controls, but this was significant only when .10% but not .05% available P was fed. The findings suggest that serum levels of both thyroid hormone and growth hormone are altered by P deficiency, but the results were not clearly definitive.

Animals↗
PubMed1985

Effect of phosphorus deficiency on thyroid function and growth hormone in the white Leghorn male.

Leghorn males, 66 to 96 days of age, were fed a diet marginally deficient in phosphorus (.14% nonphytate). Growth and feed intake were significantly reduced, but plasma calcium and phosphorus were unchanged. Bone ash was significantly reduced compared to pair-fed controls but not ad libitum-fed controls. Thyroid size increased and plasma growth hormone (GH) levels decreased with the deficiency, apart from any effect attributable to the lower food intake and weight gain. Plasma 3,5,3'triiodothyronine (T3) and thyroxine (T4) were not significantly changed, although there was a tendency for T4 to be lower in the deficient chickens. As both thyroid size and plasma GH are regulated partly by pituitary function, dietary phosphorus may alter endocrine function through changes in pituitary metabolism.

Animals↗
PubMed1983

Effect of a tryptophan deficiency on thyroid gland, growth hormone and testicular functions in chickens.

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.

Animals↗