Comments on the paper by Garwin et al. (1992)
Explore the source record for details and available documents.
Cholesterol↗
Biomedical subjects
W E Donaldson
Publications and source records attributed to W E Donaldson.
Effect of maternal dietary triiodothyronine on embryonic physiology of turkeys.
The objective of the present experiment was to feed triiodothyronine (T3) to lines of turkey breeders selected for egg production and growth, and an unselected control line. The data were collected to determine a genetic basis for thyroid-mediated maternal effects on embryonic physiology and livability. At 30 wk of age, turkeys of the three lines were photostimulated and half of each line was fed a diet containing .5 ppm T3. Maternal dietary T3 increased egg weight, reduced yolk solids and eggshell conductance constants, and increased albumen solids and water in eggs in all lines compared with control eggs. Hatchability in all lines was not affected by the dietary treatment (Control = 72.2%; T3 treatment = 70.7%), but there was a significant interaction between dietary T3 and line of turkey for the time of embryonic mortality, time of hatching, and carbohydrate metabolism of the embryo. The T3 increased mortality of the Egg line and unselected line during pipping, increased mortality of the Growth line in the plateau stage, but decreased its mortality during internal pipping. Reduced glycogen in liver as well as a reduced gluconeogenesis were evident in embryos of the two selected lines fed T3. It is concluded that genetic lines may have different metabolic patterns based on their genetic constitution in order to compensate for variations in egg solids and eggshell conductance constants. The metabolic patterns are reflected in different levels of embryonic blood plasma glucose, glycogen, and gluconeogenesis.
Animals↗
Effects of injections of L-alanine, L-glucose and L-ascorbic acid in newly-hatched turkey poults on glucose metabolism.
1. Effects of subcutaneous injections of either L-glucose, L-alanine or L-ascorbate into newly-hatched, fasted turkey poults were examined. 2. There were no effects of injections on blood glucose concentrations at 20 hr post-injection. 3. Glucose injections inhibited hepatic glucose-6-phosphatase activity while alanine injections did not. 4. Both glucose and alanine injections enhanced hepatic glycogen reserves at 20 hr post-injection.
Alanine↗
Posthatch carbohydrate feeding and subsequent performance of turkey poults.
In two floor pen trials, day-old poults were fed a low-protein (18.6%) diet for the first 24 or 48 h compared with control poults fed a 28% protein diet. Beyond these initial treatments, all poults were treated identically and were fed the normal progression of starter, grower, and finisher diets to market weight. The treatments did not alter market age body weight or feed conversion. Early mortality and feed intake during the first 48 h were unaffected by the treatments. Feeding the low-protein diet for 24 h enhanced liver glycogen reserves compared with the control. In a battery cage trial, diets containing 50, 33, or 15% available carbohydrate (20, 28, or 35% crude protein, respectively) were fed for 24 h posthatch. The diets had no effect on blood glucose level, but liver glycogen concentration increased with increasing dietary carbohydrate. The results clearly indicate that carbohydrate metabolism is altered by posthatch dietary carbohydrate level. The results also suggest that the dietary protein requirement during the first 24 or 48 h posthatch may not be as high as it is currently thought to be.
Animal Feed↗
Effect of oxygen and maternal dietary iodine on embryonic carbohydrate metabolism and hatchability of turkey eggs.
Fertile turkey eggs were produced by hens fed supplemental iodine to decrease eggshell conductance. The eggs were then incubated in an oxygen-enriched environment during Days 25 and 26 of incubation to test the hypothesis that maternal dietary iodine has separate effects on the eggshell permeability and the developing embryo. Oxygen supplementation improved hatchability regardless of dietary iodine treatment, suggesting that oxygen availability may limit hatching of eggs with normal gas conductance. Oxygen and dietary iodine did not affect body weight but interacted prior to pipping to affect embryonic liver and heart glycogen. Dietary iodine increased liver glycogen at internal pipping. The effects of oxygen on embryos, which were correlated directly with hatchability, were increased liver growth prior to pipping and increased heart weight at external pipping and posthatching. It was concluded that supplementing oxygen to incubating turkey eggs may improve hatchability by increasing liver and heart growth. Dietary iodine played only a minor or modulating role in assisting embryos to survive.
Animal Feed↗
Lead-induced tissue fatty acid alterations and lipid peroxidation.
Previous work showed that dietary lead (Pb) increases the relative concentration of arachidonic acid (20:4) as a percentage of total fatty acids, and decreases the relative proportion of linoleic acid (18:2) to arachidonic acid (18:2/20:4) in chick liver, serum, and erythrocyte membranes. The present investigation was undertaken to examine the time-course and magnitude of the fatty acid alterations with increasing dietary Pb levels. We also examined the effects of Pb on the fatty acid composition and lipid peroxide content of hepatic subcellular organelles. In Exp. 1, chicks were fed diets containing 0, 62.5, 125, 250, 500, or 1000 ppm added Pb (as Pb acetate trihydrate) from 1 to 21 d of age. After 21 d, no growth effects were observed; however, Pb lowered the 18:2/20:4 ratio and increased 20:4 concentration in total liver and serum lipids, and in total hepatic phospholipids in a dose-dependent manner. Hepatic mitochondrial membrane fatty acids were not altered, nor was there any increase in hepatic lipid peroxidation. In Exp.2, chicks were fed diets containing 0, 500, 1000, or 2000 ppm added Pb from 1 to 21 or 22 d of age. Pb depressed growth in a dose-dependent manner. In addition, Pb lowered the 18:2/20:4 ratio and increased 20:4 concentration in total liver lipids and in hepatic mitochondrial and microsomal membranes in a dose-dependent manner. Total hepatic lipid peroxidation was increased over control values by 1000 ppm Pb, and hepatic microsomal lipid peroxidation was increased by dietary Pb levels of 1000 and 2000 ppm. In Exp. 3, body weight, hepatic microsomal lipid peroxidation, and fatty acid composition were determined in 4-, 9-, 14-, 18-, and 23-d-old chicks fed 0 or 1500 ppm added Pb. Body weights of Pb-treated chicks were significantly lower than those of control chicks by day 18. Microsomal 20:4 concentration and peroxidation increased, and the 18:2/20:4 ratio decreased with age in both groups, but the changes were of greater magnitude in the Pb-treated chicks. The results suggest that some of the manifestations of Pb toxicity may be a reflection of increased concentration of 20:4 in specific membranes. Further, since the Pb-induced alterations in fatty acid composition were noted in the absence of any growth depression, we propose that fatty acid composition is more sensitive than growth rate to the presence of lead in the diet.
Animals↗
Interactions of dietary lead with fish oil and antioxidant in chicks.
Two experiments were conducted with day-old broiler chicks reared to 18 or 19 d of age. The objectives were: (1) to examine the effects of the antioxidant ethoxyquin (EQ) on peroxidation in feeds containing fish oil (FO) or lead (Pb), and (2) to determine whether systemic effects of Pb, which are attributed to tissue peroxidation, can be reversed by dietary EQ. Experiment 1 was a 2 x 2 factorial arrangement with the factors being 4% dietary cottonseed oil (CSO) vs FO and dietary Pb as lead acetate trihydrate (0 vs 1000 ppm). Feed was mixed 1 d prior to initiation of the experiment and stored at 4 degrees C until it was placed in the feeders. Experiment 2 was a 2 x 2 x 2 factorial arrangement with the factors being 3.5% dietary oil (CSO vs FO), dietary Pb (0 vs 1000 ppm), and EQ (0 vs 75 ppm). Feed was mixed 1 d prior to initiation of the experiment and held at room temperature thereafter. Growth depression by FO and Pb was less pronounced in Experiment 1 than in Experiment 2. In Experiment 2, FO and Pb increased the concentration of feed peroxide, and the increases were prevented by EQ. The growth depression by FO was completely reversed by EQ. EQ reversal of Pb-induced growth depression, although substantial, was not complete. The FO diet without Pb had a peroxide content (12.4 meq/kg feed) similar to the CSO + Pb diet (12.3 meq/kg feed); however, growth was not similar (407 vs 213 g body weight at 19 d, respectively). The results suggest that the toxic effects of Pb are mediated by peroxidative alterations both in the feed and in tissues. The ability of EQ to reverse significantly Pb effects on growth suggests a systemic action of this antioxidant.
Animals↗
Effects of stressors on blood glucose and hepatic glycogen concentrations in turkey poults.
1. The putatively stressful procedures of sexing, toe trimming, snood removal, beak trimming and injection of antibiotic solution, as performed in a commercial hatchery, elevated blood glucose levels and depressed hepatic glycogen levels in newly-hatched turkey poults. 2. The first procedure performed, cloacal sexing, was sufficient to elevate blood glucose, but all procedures were required before depression of hepatic glycogen occurred. 3. Blood glucose levels declined in both untreated (INITIAL) and fully-treated (FINAL) poults over a 24 hr holding period. 4. Hepatic glycogen declined with 24 hr holding of INITIAL poults but increased with holding of FINAL poults.
Animal Husbandry↗
Dietary carbohydrate level and glucose metabolism in turkey poults.
1. Feeding British United turkeys (BUT) and Nicholas turkeys (NT) diets with varying carbohydrate levels for 24 hr post-hatch resulted in lower hepatic glucose-6-phosphatase activity and higher plasma glucose levels as dietary carbohydrate level was increased. 2. There were no differences between the strains in liver weight or glucose-6-phosphatase activity, but BUT exhibited higher plasma glucose values than did NT at the two highest levels of carbohydrate. Plasma glucose did not differ between strains at the lowest level of carbohydrate or in fasted poults. 3. Blood glucose values were consistently higher in both strains when sampled 1 hr after initial sampling of fasted poults. 4. Both strains were able to maintain the 1 hr blood glucose levels through 24 hr when kept at approximately 37 degrees C. 5. When held at approximately 21 C for the first hour and at approximately 37 degrees C through 24 hr fasted NT were able to maintain the initial blood glucose rise while BUT were not.
Animal Feed↗
Influence of diet-mediated maternal thyroid alterations on hatchability and metabolism of turkey embryos.
Large White turkey breeder hens from a strain exhibiting poor hatchability were fed thyroid-altering diets. The following dietary treatments were fed to randomized groups of hens for 15 wk of egg laying: 1) 16.5% protein turkey breeder diet (control), 2) the control diet containing 2.1 ppm supplemental iodine, 3) the control diet containing .1% thiouracil, and 4) the control diet containing .5 ppm triiodothyronine (T3). Blood samples were taken from hatching embryos from hens fed each diet. Embryonic hearts and livers were weighted prior to and during pipping as well as after hatching. Blood plasma was analyzed for thyroxine (T4), T3, and glucose. Livers were assayed for glucose-6-phosphatase activity. Supplemental maternal dietary iodine elevated embryonic T4 concentrations prior to pipping. Dietary T3 and iodine increased hepatic glucose-6-phosphatase activity and blood plasma glucose concentration prior to pipping. Feeding thiouracil increased embryonic liver weights but decreased heart and body weights. Blood plasma T4 was elevated in embryos from hens fed thiouracil but blood glucose levels were depressed because of a lack of increased glucose-6-phosphatase activity. Feeding iodine decreased the enzyme activity at internal pipping. It is suggested from the data that maternal thyroid metabolism may influence hatchability via embryonic thyroid and carbohydrate metabolism during hatching.
Animals↗
The effect of dietary iodine on the hatchability of eggs from two commercial strains of turkeys.
Supplemental dietary iodine (3.5 mg/kg) was fed to two commercial strains [British United Turkeys (B) and Nicholas (N)] of turkey breeder hens. The basal diet contained .7 mg/kg of iodine. Observations were made on hen body weights, feed consumption, hatchability, egg weights, and egg functional characteristics to test the hypothesis that there are differences between commercial strains of turkey breeder hens in the dietary iodine requirement for reproductive success. Supplemental iodine decreased (P less than or equal to .05) functional egg characteristics of both strains. Egg production and hatchability were influenced by an interaction between strains and dietary iodine (P less than or equal to .05). In Strain B hens, egg production and hatchability declined (P less than or equal to .05) when hens were fed supplemental iodine but in Strain N hens no effects on hatchability were observed and egg production increased (P less than .05) with iodine supplementation. The decline in hatchability of eggs from Strain B hens was due to significant (P less than or equal to .05) increases in embryonic mortality during the 1st wk of incubation and during pipping. The treatments resulting in depressed hatchability caused embryos to rely more (P less than or equal to .05) on glycogenolysis than gluconeogenesis during pipping and hatching. The Strain B embryos utilized gluconeogenesis more during pipping (P less than or equal to .05) than Strain N embryos and embryos from Strain B iodine-fed hens had a lower rate of gluconeogenesis than those from hens not fed iodine. It is concluded that there are differences among strains of turkey breeder hens in their dietary iodine requirement for optimal hatchability.
Animal Feed↗
Dietary modification of lead toxicity: effects on fatty acid and eicosanoid metabolism in chicks.
1. The influence of nutrition and chronic lead (Pb) administration on the level of eicosanoids and their precursors was evaluated in serum and liver from chicks fed defined diets. 2. Dietary Pb consistently increased arachidonic acid, the arachidonate/linoleate ratio, and hepatic non-protein sulfhydryl concentration. 3. Hepatic microsomal fatty acid elongation activity was decreased by Pb. 4. Cottonseed oil, calcium and methionine interacted with Pb, affecting liver and serum fatty acid profiles. 5. Tissue levels of leukotriene C4 rose significantly with Pb or correlated with Pb-compromised body weight in only one experiment. Serum prostaglandins E2 and F2 alpha were unchanged by treatments. 6. The results suggest that an increase in precursors is not consistently reflected by tissue levels of eicosanoids.
Animals↗
Morphometric analysis of osteosclerotic bone resulting from hexachlorobenzene exposure.
Hexachlorobenzene (HCB) exposure has been shown to induce hyperparathyroidism and osteosclerosis in rats. Experiments were undertaken to investigate the effects of HCB-induced hyperparathyroidism and osteosclerosis on femur morphometry as well as femur breaking strength. Fischer 344 rats were dosed 5 d/wk for 15 wk with 0, 0.1, 1, 10, or 25 mg HCB/kg body weight. Hyperparathyroidism was produced in the two higher dose groups as reported previously (Andrews et al., 1989). Femur weight was significantly increased in the rats receiving 0.1, 1, and 25 mg HCB/kg body weight, whereas density was increased significantly at 1, 10, and 25 mg HCB/kg dose levels. Bone strength was also significantly increased at the three higher dose levels. Cross-sectional area of the midpoint of the femur was significantly increased at the 1 mg/kg HCB dose level. Cortical area and the proportion of the total area of the bone that the cortex occupied were significantly increased at the three higher dose levels. Medullary cavity area was significantly increased at the 0.1 mg/kg dose level but significantly decreased at the 2 higher dose levels of HCB. The right femur was significantly predominant to the left femur in weight, volume, and density through all dosing regimens. HCB exposure significantly altered bone morphometry and strength characteristics in the Fischer 344 rat.
Alkaline Phosphatase↗
Lipid metabolism in liver of chicks: response to feeding.
Fatty-acid synthase is an enzyme complex responsible for the synthesis of the carbon chain of fatty acids. The hepatic activity of this enzyme increases rapidly during a refeeding period following a fast. The activity of fatty-acid synthase in liver of newly hatched chicks rises in parallel with the activities of other lipogenic enzymes at the initiation of feeding. Cycloheximide, an inhibitor of protein synthesis, prevents the feeding-associated rise of other lipogenic enzymes, but not of fatty-acid synthase. Evidence is reviewed that supports the hypothesis that in fasted chicks as well as in unfed, newly hatched chicks, fatty-acid synthase exists in a catalytically less-active form, one that is activated in response to feeding.
Animals↗
Hexachlorobenzene-induced hyperparathyroidism and osteosclerosis in rats.
Hexachlorobenzene (HCB) exposure has been shown to alter the normal concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D3 in rats and to result in osteoporosis in humans. Experiments were undertaken to investigate the effects of HCB on the homeostatic mechanism of calcium metabolism and to determine its effect on bone in rats. Fischer 344 rats were dosed 5 days/week for 5, 10, or 15 weeks with 0, 0.1, 10.0, or 25.0 mg HCB/kg body wt. Body weight was not affected by any of the exposure conditions. Liver weight was significantly elevated above control values at the two higher dose levels at all three time periods. Kidney weight and kidney-to-body weight ratio were significantly elevated at the highest dose level after 10 weeks and at the two higher dose levels after 15 weeks of exposure. Serum alkaline phosphatase was significantly decreased at the two higher dose levels after both 10 and 15 weeks of exposure. 1,25-Dihydroxyvitamin D3 was measured in the 5-week exposure group only and was significantly elevated in the three higher dose levels. After 5 and 15 weeks of HCB exposure, parathyroid hormone concentration was significantly elevated at the two higher dose levels at both time periods. Wet femur density was significantly increased at the two higher dose levels of HCB after 10 weeks of exposure and the three higher dose levels after 15 weeks of exposure. Dry femur density was also increased in the cases where wet femur density was increased. However, femur weight was not affected at any dose level. The results from this study indicate that HCB induces hyperparathyroidism in rats, as demonstrated by increased serum parathyroid hormone levels and osteosclerosis of the femur.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Impairment of calcium homeostasis by hexachlorobenzene (HCB) exposure in Fischer 344 rats.
Human exposure to hexachlorobenzene (HCB) has resulted in demineralization of bone and development of osteoporosis. Experiments were undertaken to investigate the effects of HCB on the homeostatic mechanism of calcium metabolism. Fischer 344 rats were dosed with 0, 0.1, 1.0, 10.0, or 25.0 mg HCB/kg body weight 5 d/wk for 5 wk while being fed normal rat diet or vitamin D3-deficient diet. Rats receiving the normal diet had a dose-related decrease in body weight gain and increased liver weight when compared to their controls. Serum cholesterol, alanine aminotransferase (ALT), 1, 25-dihydroxy-vitamin D3 [1,25-(OH)2D3], and parathyroid hormone (PTH) were significantly elevated when compared to control values. In the vitamin D3-deficient diet group, there was a dose related increase in liver weight, liver-to-body weight ratio and kidney-to-body weight ratio. Serum cholesterol and 1,25-(OH)2D3 were significantly elevated. Urinary calcium decreased significantly with increasing HCB dosage, indicating conservation of calcium. The data from this study indicate that HCB does affect calcium metabolism by altering the concentrations of two primary controlling factors in calcium homeostasis.
Alanine Transaminase↗
Effect of lead and niacin on growth and serotonin metabolism in chicks.
Interactions of lead and niacin were studied in growing broiler chicks fed one of four experimental diets from day-old to 3 wk of age. The diets were a low niacin basal diet (LN), the basal diet supplemented with 40 mg of niacin/kg (control), the basal diet supplemented with 2000 mg lead/kg, as lead acetate (LN + Pb) and the basal diet supplemented with both niacin and lead (control + Pb). Growth and feed efficiency were reduced significantly by lead. The lead-associated growth depression was less severe in chicks fed the low niacin diet as indicated by a significant lead X niacin interaction. The relative weights of two brain regions (telencephalon and diencephalon) and the adrenal glands were greater in lead-treated chicks than in their nonlead-treated counterparts. Plasma and telencephalon tryptophan were lower in lead-treated chicks than in nonlead-treated chicks. Diencephalon tryptophan was lower in chicks fed the LN diet than in chicks fed the control diet. Brain serotonin was lower and 5-hydroxyindoleacetic acid was higher in both brain regions of lead-treated chicks than in nonlead-treated chicks. The data indicate that tryptophan and serotonin metabolism were altered by lead treatment, whereas niacin was without effect. The interaction of lead and niacin on growth does not appear to be related to alterations of serotonin metabolism in the central nervous system.
Adrenal Glands↗
Effects of lead and niacin on tryptophan and serotonin metabolism.
Studies were conducted to investigate the effects of lead and niacin on tryptophan and serotonin metabolism in growing broiler chicks. A low-niacin basal diet based on soybean meal and glucose was supplemented with either 40 ppm niacin/kg feed or 2,000 ppm lead, as lead acetate trihydrate, or a combination of the two in a 2 x 2 factorial arrangement. The experimental diets were fed from 1 day to 3 weeks of age. The activities of several enzymes involved in tryptophan and serotonin metabolism were assayed in chicks fed each of the experimental diets. Lead reduced the activity of liver tryptophan pyrrolase but had no effect on the activity of hepatic picolinic carboxylase. Low dietary niacin had no effect on the activity of either of these enzymes. Brainstem tryptophan 5-hydroxylase activity was unaltered by either lead or niacin. Brain and liver monoamine oxidase activity was reduced by lead but was not affected by niacin. No interactions of lead and niacin were observed with any of the enzymes examined. Lead had no consistent effect on brain serotonin (5-HT) steady-state level, but it increased the level of the major metabolite of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA). Monoamine oxidase blockade failed to reduce the elevated 5-HIAA level in lead-treated chicks. The drug probenecid produced an increase in 5-HIAA that was comparable to the increase caused by lead. The effects of probenecid and lead were additive. It is concluded that lead significantly altered the activity of several enzymes involved with tryptophan metabolism, whereas the dietary niacin levels employed were without effect. Additionally, lead caused the accumulation of 5-HIAA in the brain, which appeared to result from inhibition of the probenecid-sensitive acid transport system.
Animals↗