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Biomedical subjects

W G Pond

Publications and source records attributed to W G Pond.

At least 127 records · Page 7Linked to original sources
PubMed1980

Selenium retention in tissues of swine fed carcasses of pigs grown on diets containing sodium selenite or high selenium white sweet clover grown on fly ash.

Growing pigs were fed diets containing 5 or 10% white sweet clover, and 0, 3.5 or 7.0 ppm selenium (Se) supplied as sodium selenite (Na2SeO3) or occurring naturally in white sweet clover harvested from a coal fly ash dump. Ground carcasses of these pigs were included in corn meal diets at 23% and fed back to pigs. Compared to the pigs fed the high Se, fly ash-grown clover diets, the pigs fed Na2SeO3 diets had higher blood Se levels but lower Se concentrations in kidney, liver and skeletal muscle. Tissues of the pigs which were fed carcasses of the high Se clover-fed pigs had higher Se concentrations than those of the pigs fed carcasses of the Na2SeO3 - fed pigs.

Animal Feed↗
PubMed1978

Vitamin D toxicity. Initial site and mode of action.

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.

Animals↗
PubMed1977

Food intake controls in the suckling pig: glucoprivation and gastrointestinal factors.

The energy balance of suckling Yorkshire pigs 1 day to 2 wk old was challenged by: food deprivation, glucoprivation, and caloric and noncaloric gastric loads delivered by intubation. tafter 2--4 h fasts, food intake greatly increased over nonfasted control intake during a 3-h refeeding period. This response occurred both when body weight gain was used as a measure of intake for pigs nursing on the sow and when intake was measured directly in bottle-fed pigs. Glucoprivation produced by 0.5--2 U/kg insulin did not stimulate food intake although plasma glucose fell to a mean of 49 mg/100 ml (43% of control) after 1 U/kg insulin. Gastric loads of water or 3% NACl depressed intake after 3-h fast, but 0.9% NaCl did not. All the caloric gastric loads depressed intake; in order of increasing effectiveness, they were: heavy cream, protein hydrolysate, corn oil, milk, 5% glucose, and 5% lactose. The carbohydrate loads were most effective, a result which indicates that the response was not to calories alone but to some specific nutrient, possibly glucose.

Animals↗
PubMed1977

Cestrum diurnum intoxication in normal and hyperparathyroid pigs.

The effect of ingestion of dried leaves of Cestrum diurnum, a plant shown to contain a 1,25-dihydroxycholecalciferol-like principle, was tested in normal pigs fed 1.2% calcium and 1.0% phosphorus for 10 weeks from weaning and in hyperparathyroid pigs fed 0.8% calcium and 1.6% phosphorus for the same periods of time. Addition of 3% Cestrum diurnum leaf meal rapidly resulted in decreased feed consumption and weight gain, hypercalcemia and hypophosphatasemia. In normal pigs, plasma calcium rose to 16 mg/100 ml within one week and remained high for the 4 week experimental period. In hyperparathyroid pigs with hypocalcemia, plasma calcium rose to 12.75 mg/100 ml within one week and later approached 15 mg/100 ml. Ingestion of Cestrum diurnum retarded cell differentiation of growth cartilages. Arrested osteocytic osteolysis was observed within one week with osteopetrosis of epiphyses and metaphyses. The negative effect on the resorbing osteocytes then caused osteonecrosis which, in combination with lack of bone formation because of atrophy of osteoblasts, resulted in osteopenia within 4 weeks. Dystrophic calcinosis occurred within 2 weeks and was widespread after 4 weeks in lungs, kidneys, heart and vessels. Atrophy of parathyroid cells was severe after one week. Hyperparathyroid pigs responded with skeletal lesions, dystrophic calcinosis and parathyroid atrophy more rapidly and severely than normal pigs. The biochemical and anatomical changes in Cestrum diurnum ingestion are closely similar to those in vitamin D3 intoxication in pigs. Whereas pigs can tolerate large amounts of vitamin D3 because of feed-back control of 1 alpha-hydroxylation in the kidney, this control point is by-passed in Cestrum diurnum ingestion and intoxication occurs promptly.

Alkaline Phosphatase↗
PubMed1976

Effect of postnatal dietary protein and energy restriction on exploratory behavior in young pigs.

Three-week-old pigs were subjected to dietary energy or protein restriction so as to prevent weight gain over a period of 8 weeks. During the last week of restriction their responses to a novel object introduced into an exploratory test situation were measured. The malnourished pigs exhibited indifference to the object, taking longer to make contact with it, spending less time playing with it, but not showing evidence of fear or avoidance of the object or the area in which it was located. Following 6 weeks of nutritional rehabilitation, the previously malnourished pigs again displayed less approach behavior to the novel object than controls, but the effect was substantially reduced. These observations are interpreted to support our hypothesis that a major mechanism through which early malnutrition produces long-term effects on behavior is by disturbing those behaviors required for gathering information from the environment.

Animals↗
PubMed1976

Maternal protein malnutrition during gestation alone and its effects on plasma insulin levels of the pregnant pig, its fetuses and the developing offspring.

The effects of restricting protein intake on plasma insulin were studied in pregnant pigs, fetuses and the developing offspring. Pregnant pigs were fed diets containing 18%, 3% or 0.5% protein throughout the gestation period. At 10, 13 and 15 weeks of gestation, fetuses were removed from the uterus after bleeding the dam. Plasma samples were used for insulin determination by a radioimmunoassay procedure. At week 15 of gestation, plasma insulin levels were significantly higher in pregnant pigs fed 18% protein and also in their fetuses than in the other two groups. There was a high correlation between fetal insulin level and fetal growth rate (r = 0.84). Two-day-pld pigs from another set of pregnant pigs fed the diet containing 18%, 3%, or 0.5% protein during gestation were cross-fostered to control nursing dams and weaned at 4 weeks of age to a standard diet. Plasma smaples obtained at regular intervals were used for insulin determination. Offspring of pigs fed 0.5% protein during gestation had consistently low insulin levels in postnatal life in spite of cross-fostering and standard feeding after weaning. It appears that one of the stimuli which control maternal insulin secretion and placenta transfer is the maternal protein intake while severe maternal protein restriction might contribute to the low levels of insulin in the progeny during postnatal life.

Animals↗
PubMed1976

Plasma insulin levels in weaned pigs fed protein or energy restricted diets.

Two experiments were conducted with pigs to investigate changes in plasma insulin levels during protein-energy malnutrition. Three or four week old pigs were fed a control diet (18% protein), an energy-restricted diet (19% protein) or a low protein diet (6% protein) for 8 weeks. Energy restriction was achieved by feeding the control diet in amounts that allowed some growth, but only to an extent equal to the low protein diet. At the end of the restriction period, all pigs were fed the control diet for another 8 weeks. Blood samples from the superior vena cava were collected at intervals throughout the experimental period. Plasma samples were analyzed for insulin by radioimmunoassay. Protein restriction after weaning resulted in persistently low insulin levels during depletion and rehabilitation periods, while high levels of plasma insulin were observed in energy-restricted pigs only during the depletion period compared to pigs fed the control diet.

Animals↗
PubMed1976

Decreased dietary protein or energy intake and plasma growth hormone levels of the pregnant pig, its fetuses and developing progeny.

The effects of low protein diets on plasma growth hormone were studied in pregnant pigs, fetuses and the developing progeny. Pregnant pigs were fed 18%, 3% or 0.5% protein diet throughout the gestation period. At 10, 13 and 15 week of gestation, fetuses were removed from the uterus after the dam had been bled to death. Plasma samples were used for growth hormone determinations. In a second experiment, 2-day old pigs from another set of pregnant pigs fed the diet containing 18%, 3% or 0.5% protein during gestation were cross-fostered to control nursing dams and weaned at 4 weeks of age to a standard diet. Plasma obtained at regular intervals was used for growth hormone determination. Plasma growth hormone was significantly higher in dams fed 0.5% protein after week 13 of gestation. High growth hormone (ten times the dam GH level) was observed in all fetuses irrespective of maternal dietary manipulation. Offspring of severely protein deprived pits (0.5% protein) had significantly elevated growth hormone levels up to 12 weeks of age in spite of cross fostering to a control dam after birth. The data suggest that there is little or no effect of maternal protein restriction on fetal growth hormone levels but the persistent high growth hormone levels in the progeny of severely malnourished pigs indicate a possible impairment of the production, release or catabolism of growth hormone and/or its releasing factor.

Animals↗