Impact of amino acid nutrition during lactation on luteinizing hormone secretion and return to estrus in primiparous sows.
(25/2537)
The impact of the dietary amino acid regimen of primiparous sows on LH secretion and weaning-to-estrus interval was evaluated. Thirty-six sows, nursing litters of 13 pigs, were allocated daily 6 kg of a corn-soybean meal diet containing a high (HP, 1.20% lysine) or low (LP, .34% lysine) protein content during a 23-d lactation. Dietary lysine concentration was achieved by altering the ratio of corn and soybean meal in the diet. Plasma LH, ACTH, and estradiol-17beta were evaluated at 15 min, hourly, and at 6-h intervals, respectively, during 6-h periods on d 0, 5, 10, 15, and 20 of lactation. Sows were checked daily for estrus from weaning to 45 d postweaning. Sows fed the LP and HP diets consumed 4.41 and 4.98 kg of feed daily during lactation. The LP sows weighed less (P < .05), had lighter (P < .05) litters at weaning, and had (P < .05) extended weaning-to-estrus intervals. Mean and baseline LH concentrations and LH pulses/6 h were lower (P < .01) in LP sows, and the differences between LP and HP sows were established by d 10 of lactation. Plasma estradiol and ACTH concentrations were not altered by diet. Mean LH concentrations on d 5 and 10 of lactation were correlated (r = -.54 and -.56, respectively, P < .01) with weaning-to-estrus interval. Also, mean LH concentrations on d 10 were correlated (P < .05) with the magnitude of dietary lysine deficiencies relative to demand for milk synthesis on d 0 to 5 and d 5 to 10 (r = -.39 and -.49, respectively). Inadequate dietary amino acid intake in sows during early lactation results in lower LH secretion by d 10 postpartum and is associated with increased weaning-to-estrus interval. (+info)
Failure of vitamin A to increase litter size in sows receiving injections at various stages of gestation.
(26/2537)
To determine the effectiveness of a single injection of vitamin A to increase litter size, 1,375 sows were assigned randomly to 11 treatment groups (125 sows per treatment). Treatments included injection of 1 x 10(6) IU of vitamin A dissolved in corn oil at weaning or on d 0, 2, 6, 10, 13, 19, 30, 70, or 110 after breeding. Sows in the control group were injected with corn oil on corresponding days. A total of 396 sows were removed from the study following treatment or treatment assignment. Therefore, farrowing data were collected for 979 sows. Injection of vitamin A did not influence (P > . 10) total litter size, live litter size, litter weight, pig weight, number of runts, or number of mummies. Mean live litter size was 10.1 +/- .1 for all sows that farrowed in the experiment. Parity group affected total litter size, live litter size, live litter weight, and number stillborn (P < .01) but not pig weight, number of runts, number of mummies, or gestation length (P > . 10). In this study, a single injection of vitamin A at any time from weaning to farrowing did not increase litter size in sows. (+info)
The impact of mammalian reproduction on cancellous bone architecture.
(27/2537)
Pregnancy and lactation make demands on maternal calcium homeostasis which may affect bone strength. Recently, changes in cancellous architecture have been described in iliac crest bone biopsies from normal pregnant women but the rarity of such human material means an animal model is essential. The microanatomy of cancellous bone was compared in uniparous and multiparous rats using undecalcified histological sections of lumbar and caudal vertebrae and also proximal femora. An automated trabecular analysis system (TAS) measured a comprehensive range of structural variables including the trabecular number, connectivity and width. In the first pregnancy cycle an early stimulation of bone formation (which quadrupled at some sites) was indicated by an increase in the skeletal uptake and spacing of double calcein labels and the immediate generation of thicker more numerous and interconnected trabeculae. A 40% increase in cancellous bone volume was observed in the lumbar spine in comparison with age-matched virgin controls. In contrast, a rapid succession of 3 pregnancy cycles (including lactation) culminated in cancellous atrophy of 15% at the same site, with a loss in trabecular number ranging from 20% (caudal vertebra) to 30% (lumbar vertebrae). In comparison, the proximal femur lost 40% of its struts but, nevertheless, uniquely sustained its cancellous bone volume. When lactation was excluded the number of struts lost was halved although trabecular thinning then took place which was sufficient to maintain the previous 15% deficit in bone volume. It was concluded that a single pregnancy strengthens the cancellous component of the maternal skeleton while a quick succession of pregnancies weakens it. Lactation influences the pattern of bone loss but not its amount. (+info)
Previous maternal abortion, longer gestation, and younger maternal age decrease the risk of type 1 diabetes among male offspring.
(28/2537)
OBJECTIVE: To identify possible influences and interactions of perinatal determinants in the subsequent development of type 1 diabetes. RESEARCH DESIGN AND METHODS: The data were obtained from children born in Denmark during the periods 1978-1982 and 1984-1986 and admitted to a Danish hospital with newly diagnosed type 1 diabetes between 1978 and 1995; 857 patients fulfilled the criteria. The study was conducted by combining and analyzing two national registries: the National Patient Registry and the Medical Birth Registry. For each diabetic child, two control children were randomly selected, matched by sex, time, and district of delivery. RESULTS: By multivariate logistic regression analysis, the following significant determinants were identified. Male offspring showed decreased risk when born of mothers who had had one or more abortions (odds ratio [OR] 0.66 [95% CI 0.48-0.92]) and with long duration of gestation (linearly with OR 0.91 per week [0.85-0.99]), while increased risk was found for high maternal age (linearly with OR 1.03 per year [1.00-1.06]). Female offspring showed no such association. No significant differences between diabetic patients and control subjects were found with respect to paternal age, maternal parity, placental weight or any of the birth size parameters, or interventions and complications during delivery. CONCLUSIONS: The findings show that perinatal determinants may influence the risk of subsequent development of type 1 diabetes in a sex-specific manner. (+info)
Preterm delivery and risk of breast cancer.
(29/2537)
To explore the risk of breast cancer in relation to the length of a pregnancy we tested whether a preterm delivery carries a higher risk of breast cancer than does a full-term delivery. Based on information from the Civil Registration System, and the National Birth Registry in Denmark, we established a population-based cohort of 474 156 women born since April 1935, with vital status and detailed parity information, including the gestational age of liveborn children and stillbirths. Information on spontaneous and induced abortions was obtained from the National Hospital Discharge Registry and the National Registry of Induced Abortions. Incident cases of breast cancer in the cohort (n = 1363) were identified through linkage with the Danish Cancer Registry. The period at risk started in 1978 and continued until a breast cancer diagnosis, death, emigration, or 31 December, 1992, whichever occurred first. After adjusting for attained age, parity, age at first birth and calendar period, we observed the following relative risks of breast cancer for different lengths of the pregnancy: < 29 gestational weeks = 2.11 (95% confidence interval 1.00-4.45); 29-31 weeks = 2.08 (1.20-3.60); 32-33 weeks = 1.12 (0.62-2.04); 34-35 weeks = 1.08 (0.71-1.66); 36-37 weeks = 1.04 (0.83-1.32); 38-39 weeks = 1.02 (0.89-1.17); 40 weeks = 1 (reference). Parous women who had a preterm delivery below 32 weeks gestation had a 1.72-fold (1.14-2.59) increased risk of breast cancer compared with other parous women. In conclusion, a preterm delivery of 32+ weeks gestation did not significantly increase a woman's risk of contracting breast cancer. Only for the very small group of women with preterm deliveries of less than 32 weeks gestation did we observe an increased risk. (+info)
Maternal zinc supplementation does not affect size at birth or pregnancy duration in Peru.
(30/2537)
To estimate the effect of maternal zinc deficiency on pregnancy outcomes, we conducted a zinc supplementation trial in an urban shantytown in Lima, Peru, a population with habitual low zinc intakes. Beginning at 10-24 wk gestation, 1295 mothers were randomly assigned to receive prenatal supplements containing 60 mg iron and 250 (g folate, with or without 15 mg zinc. Women were followed up monthly during pregnancy. At birth, newborn weight was recorded, and crownheel length, head circumference and other circumferences and skinfold thicknesses were assessed on d 1. At delivery, 1016 remained in the study; duration of pregnancy was known for all women, and birth weight information was available for 957 newborns. No differences were noted in duration of pregnancy (39.4 +/- 2.2 vs. 39. 5 +/- 2.0 wk) or birth weight (3267 +/- 461 vs. 3300 +/- 498 g) by prenatal supplement type (iron + folate + zinc vs. iron + folate; P > 0.05), and there were no differences in the rates of preterm (<37 wk) or post-term (>42 wk) delivery, low birth weight (<2500 g) or high birth weight (>4000 g). Finally, there were no differences by prenatal supplement type in newborn head circumference, crownheel length, chest circumference, mid-upper arm circumference, calf circumference or skinfold thickness at any of three sites. Adjustment for covariates and confounding factors did not alter these results. Adding zinc to prenatal iron and folate tablets did not affect duration of pregnancy or size at birth in this population. (+info)
Developmental toxicity studies of 2-(difluoromethyl)-dl-ornithine (DFMO) in rats and rabbits.
(31/2537)
DFMO, an irreversible inhibitor of ornithine decarboxylase (ODC), is under development as a chemopreventive drug against cancers with pronounced proliferative phases. In support of human clinical trials, preclinical developmental toxicity studies were conducted in pregnant rats and rabbits. Rats were treated during GD 6-17, and fetuses were obtained by C-section on GD 20. Rabbits were treated during GD 7-20, and fetuses were obtained by C-section on GD 29. The dose range-finding study in rats (5/group at 0, 50, 125, 300, 800, or 1000 mg/kg/day) revealed maternal toxicity at doses > or = 800 mg/kg/day (decreased body weights and food consumption) and developmental toxicity at doses > or = 300 mg/kg/day (increased early resorptions and reduced fetal body weights). In the main study, rats (25/group) received 0, 30, 80, or 200 mg/kg/day. Developmental toxicity in the absence of maternal toxicity was observed at 200 mg/kg/day as significantly decreased fetal weights and increased incidence of litters with skeletal variations of 14th rudimentary rib, 14th full rib, and/or 27th presacral vertebrae. There were no treatment-related fetal skeletal malformations or external or visceral anomalies at any dose level. The dose range-finding study in rabbits (5/group at 0, 30, 60, 120, 240, or 500 mg/kg/day) revealed developmental toxicity at doses > or = 60 mg/kg/day (increased resorptions and reduced fetal body weights) in the absence of maternal toxicity. In the main study, rabbits (20/group) received 0, 15, 45, or 135 mg/kg/day. Developmental toxicity in the absence of maternal toxicity was observed at 135 mg/kg/day as nonsignificantly increased early resorptions, decreased implantation sites, decreased viable fetuses, and reduced fetal weights. There were no external, visceral, or skeletal anomalies at any dose level. Thus, in the main developmental toxicity studies, DFMO produced developmental but not maternal toxicity at 200 and 135 mg/kg/day in rats and rabbits, respectively. Accordingly, in rats, the maternal no-observable-effect level (NOEL) was 200 mg/kg/day and the fetal NOEL was 80 mg/kg/day; while in rabbits the maternal NOEL was 135 mg/kg/day and the fetal NOEL was 45 mg/kg/day. These fetal NOELs are several-fold higher than the dose level currently used in Phase II and III clinical trials (approximately 13 mg/kg). (+info)
Developmental toxicities of methacrylic acid, ethyl methacrylate, n-butyl methacrylate, and allyl methacrylate in rats following inhalation exposure.
(32/2537)
The developmental toxicities of 4 methacrylates were studied in Sprague-Dawley rats after inhalation exposure for 6 h/day, during days 6 to 20 of gestation. The exposure concentrations were, for methacrylic acid, 0, 50, 100, 200, or 300 ppm; for ethyl methacrylate, 0, 600, 1200, 1800, or 2400 ppm; for n-butyl methacrylate, 0, 100, 300, 600, or 1200 ppm; and for allyl methacrylate, 0, 12, 25, 50, or 100 ppm. No significant increases in embryo/fetal lethality or fetal malformations were observed after exposure to any of these methacrylates. Fetal toxicity evidenced by statistically significant decreases in fetal body weights was observed at exposure levels > or = 1200 ppm ethyl methacrylate, > or = 600 ppm n-butyl methacrylate, and at 100 ppm allyl methacrylate. Statistically significant increases in the incidence of fetuses with skeletal variations and of fetuses with any variations were noted at 1200 ppm n-butyl methacrylate. These developmental effects were observed in the presence of overt signs of maternal toxicity. While maternal toxicity was observed, methacrylic acid caused no evidence of developmental toxicity up to 300 ppm. (+info)