Changes in the relationship between porcine fetal size and organ development during pregnancy

2000 ◽  
Vol 2000 ◽  
pp. 123-123
Author(s):  
P. F. N. Silva ◽  
A. M. Finch ◽  
C. Antipatis ◽  
C. J. Ashworth

Individual piglet birthweight is a major determinant of subsequent survival and weaning weight of the litter. Low birthweight piglets are more likely to die from starvation and thermoregulatory stress than their heavier littermates, while those that do survive grow more slowly and reach a lower mature body weight with a higher body fat to muscle ratio. Inadequately grown porcine fetuses are often characterised by assymetrical organ development although it is not clear when this difference in relative organ size arises and whether this is a consequence of changes in cell size or cell number. The objectives of this study were to assess a range of determinants of fetal growth at stages of gestation and to determine when changes in the relationship between fetal size and organ development occur.

1981 ◽  
Vol 240 (1) ◽  
pp. E72-E78 ◽  
Author(s):  
M. R. Greenwood ◽  
M. P. Cleary ◽  
R. Gruen ◽  
D. Blase ◽  
J. S. Stern ◽  
...  

Young Zucker lean (Fa/-) and obese (fa/fa) female rats were fed the fatty acid synthesis inhibitor (-)-hydroxy-citrate as a dietary admixture for 39 days. In the lean rats, (-)-hydroxycitrate treatment decreased body weight, food intake, percent of body fat, and fat cell size. In the obese rat, food intake and body weight were reduced but the percent of body fat remained unchanged. Throughout the treatment period, obese rats maintained a fat cell size equivalent to their obese controls. Although a reduction in fat cell number in the obese rats occurred during the treatment period, marked hyperplasia was observed during the posttreatment period. The results of this study indicate that the obese rat, despite a substantial reduction in body weight produced by (-)-hydroxycitrate, still defends its obese body composition.


1997 ◽  
Vol 48 (6) ◽  
pp. 743 ◽  
Author(s):  
D. M. McNeill ◽  
R. W. Kelly ◽  
I. H. Williams

The effect of ewe fatness on fetal weight at term was tested without the confounding effects of placental weight and feed intake. We hypothesised that fetal weights should be similar in fat or lean ewes with placentas of a similar size, and tested the hypothesis by manipulating nutrition so that, at mating, Merino ewes carrying a single fetus were in a medium (score 2·9, liveweight 46·6 kg) or lean (score 2·0, liveweight 40·6 kg) condition. They were maintained at this fatness difference until slaughter at Day 146 of pregnancy when fetal, placental, and maternal tissues were weighed and analysed for composition. Subgroups (n = 8 per fatness group) slaughtered at Day 110, a stage when most placental hypertrophy is complete but the majority of fetal hypertrophy is yet to occur, confirmed that the treatments differed in ewe fatness (3·82 v. 9·19 kg empty-body fat, s.e.m. = 0·960; P < 0·001) but not placental weight (487 v. 538 g, s.e.m. = 41·5, P > 0·05). By Day 146, fatness differences (4·77 v. 9·56 kg empty-body fat, s.e.m. = 0·960, P < 0·001) and placental similarities (434 v. 502 g, s.e.m. = 38·3, P > 0·05) were maintained, and both groups produced fetuses of similar size (4408 v. 4382 g, s.e.m. = 204·6, P > 0·05). However, the fetuses in the lean ewes had 20% less fat/kg fat-free body weight (24 v. 30 g/kg, s.e.m. = 1·3, P < 0·01). Fetal weight was correlated with placental weight (r = 0·70; P < 0·01) but not with ewe fatness. Fetal fatness, however, was correlated with ewe fatness (r = 0·69; P < 0·01). Ewe fatness per se did not influence fetal size but did influence the deposition of fat in the fetus, possibly via a greater ability of fatter ewes to partition more glucose toward their fetus.


2021 ◽  
Vol 2 (1) ◽  
pp. 19
Author(s):  
Suci Eka Putri ◽  
Adelina Irmayani Lubis

Body mass index (BMI) is to monitor nutritional status adults, especially those related to deficiency and overweight. Body fat percentage can describe the risk of degenerative diseases.This study was conducted to measure the relationship between BMI and body fat percentage. Methods An analytical study was conducted to 41 male and 51 female participant from Universitas Teuku Umar. The body weight was measured using scales, whereas the body height was measured using microtoise. The body fat percentage was measured using Karada Scan. The BMI was calculated by dividing the body weight in kilogram divided by body height in meter square. Data was collected from 16-18th February 2021 and analyzed by Pearson’s correlation test. The results showed BMI underweight, normal, and overweight were 10,9, 57,6, and 31,5. High body fat percentage in men were 75,6% and in women were 35,5%. There is a relationship between the nutritional status of the women group and the body fat percentage with p-value is obtained = 0.021. Furthermore, for men, there is no relationship between nutritional status in the men group and the body fat percentage. There is a relationship between nutritional status and body fat percentage in women. Among this population, BMI can still be used to determine body fat percentage


Development ◽  
1985 ◽  
Vol 88 (1) ◽  
pp. 183-192
Author(s):  
Rudolf Winklbauer ◽  
Peter Hausen

During normal development of the supraorbital lateral line system of Xenopus, an elongated streak of primordial cells becomes subdivided into a linear series of cell groups containing only about eight cells each, thus forming a row of primary lateral line organs (Winklbauer & Hausen, 1983a,b). In triploid Xenopus embryos, cell size is 1·5 × normal. When the formation of lateral line organs occurs in triploid primordia, the nascent organs contain only about five or six cells each, i.e. about two thirds of normal. Thus, the increase in cell size is compensated for by a corresponding reduction in cell number, keeping constant the organ size in terms of total cell mass or volume. This result excludes a cell counting mechanism for determining organ size. In diploids, the primary organs, although being of equal size initially, differ vastly in their final size and exhibit a peculiar frequency distribution of organ sizes. A detailed quantitative model for supraorbital lateral line development has been proposed, which accounts for this characteristic frequency distribution (Winklbauer & Hausen, 1983b). This model makes precise predictions as to the frequency distribution of the final size of triploid lateral line organs, where the initial organ size is reduced to five or six cells. These predictions were verified experimentally.


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Sandra L Rebholz ◽  
John T Melchior ◽  
Jeff Welge ◽  
Andrew M Prentice ◽  
Sophie E Moore ◽  
...  

Babies born with low birthweight are often at a health disadvantage. Previous studies have shown direct relationships between maternal plasma cholesterol and infant birthweight in resource-rich countries. As plasma cholesterol levels are often decreased in resource-poor countries, the purpose of these studies was to evaluate the relationship between plasma cholesterol and birthweight in women enrolled in the ENID trial (ISRCTN49285450) in rural Gambia, West Africa. Plasma was obtained at enrolment (13.6±3.3 wk) and at 20 and 30 weeks of gestation; samples were obtained from women with term infants that weighed <2.75 kg or >3.25 kg at birth. Women with lower HDL-cholesterol (HDL-C) concentrations in mid-pregnancy had lower birthweight infants compared to women with higher HDL-C concentrations. There was no significant association between LDL-C or total cholesterol concentrations and birthweight. The relationship with HDL-C and birthweight was maintained when maternal BMI was included in the model. To begin to elucidate the processes involved in the regulation of fetal growth, placental function was examined in mice with increasing maternal HDL-C concentrations based on apoA-I levels; mice were lacking apoA-I (apoA-I -/- ), were wildtype (apoA-I +/+ ), or had excess apoA-I (apoA-I tg/tg ). HDL decreased in size as plasma apoA-I levels increased, and there were no statistical differences in the proteins carried by HDL, except for apoA-I, in pregnant mice of different genotypes. However, pregnancy alone led to changes in the HDL proteome. Importantly, fetuses of mice with lower concentrations of maternal HDL-C had reduced growth rates, not due to a lack of fetal apoA-I. The murine fetal growth rates were directly related to nutrient uptake by and transport across the placenta. This work suggests that maternal HDL affects placental function leading to enhanced nutrient supply and improved growth in utero, making HDL a potential biomarker for fetal growth and putative target for intervention.


1989 ◽  
Vol 257 (5) ◽  
pp. R1128-R1135 ◽  
Author(s):  
D. S. Lewis ◽  
H. A. Bertrand ◽  
C. A. McMahan ◽  
H. C. McGill ◽  
K. D. Carey ◽  
...  

The hypothesis that infant overnutrition increases fat cell number and promotes obesity in the young adult primate was tested. Newborn baboons were fed similar volumes of Similac formulas with caloric densities of 40.5 (underfed, n = 8), 67.5 (normally fed, n = 12), and 94.5 (overfed, n = 12) kcal/100 g formula until 4 mo of age. Afterwards all baboons were fed the same diet until they were young adults. At 5 yr of age body composition, mean fat cell size, and total fat cell number were measured. Infant food intake did not significantly influence body composition or fat cell number in the 5-yr-old male baboons. Five-year-old female baboons, overfed as infants, had significantly greater body fat mass, percent of body mass that was fat, and mean fat cell volume compared with females that were underfed or normally fed as infants. There was no difference in total fat cell number between the obese baboons that were overfed as infants and the lean baboons that were underfed or normally fed as infants. Fat cell number was not associated with body fat content; males had more fat cells than did females. These results demonstrate that infant overnutrition in a primate species promotes obesity in young adult females by increasing primarily fat cell size and not fat cell number.


2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Harry Freitag Luglio Muhammad ◽  
Dian Caturini Sulistyoningrum ◽  
Emy Huriyati ◽  
Yi Yi Lee ◽  
Wan Abdul Manan Wan Muda

Background. Coffee is suggested as an alternative option for weight loss but the relationship between coffee consumption and adiposity in population-based studies is still controversial. Therefore, this study was aimed at evaluating the relationship between coffee intake and adiposity in adults and to test whether uncoupling protein 2 (UCP2) gene variation was able to affect this relationship. Methods. This was a cross-sectional study conducted in male and female adults living in the urban area of Yogyakarta, Indonesia. Adiposity was determined based on body weight, body mass index (BMI), percent body fat, and waist and hip circumference. Data on coffee consumption and other dietary components were collected using a semiquantitative food frequency questionnaire along with other caffeine-containing beverages such as tea, chocolate, and other beverages. The −866 G/A UCP2 gene variation was analyzed using polymerase chain reaction-restriction fragment length polymorphism. The correlation between coffee intake and adiposity was tested using linear regression test with adjustment for sex, age, energy intake, table sugar intake, and total caffeine intake. Results. In all subjects, coffee intake was inversely correlated with body weight (β = −0.122, p=0.028), BMI (β = −0.157, p=0.005), and body fat (β = −0.135, p=0.009). In subjects with AA + GA genotypes, coffee intake was inversely correlated with body weight (β = −0.155, p=0.027), BMI (β = −0.179, p=0.010), and body fat (β = −0.148, p=0.021). By contrast, in subjects with GG genotype, coffee intake was not correlated with body weight (β = −0.017, p=0.822), BMI (β = −0.068, p=0.377), and body fat (β = −0.047, p=0.504). Conclusion. We showed that coffee intake was negatively correlated with adiposity, and this was independent of total caffeine intake. Additionally, we showed that the −866 G/A UCP2 gene variation influences the relationship between coffee intake and adiposity.


2002 ◽  
Vol 14 (7) ◽  
pp. 419 ◽  
Author(s):  
A. M. Finch ◽  
C. Antipatis ◽  
A. R. Pickard ◽  
C. J. Ashworth

Low birthweight piglets have an increased incidence of mortality and morbidity. As there are few opportunities to remedy the detrimental consequences of low birthweight after birth, it is important to understand the nature of fetal growth retardation and to identify when low birthweight fetuses deviate from the growth trajectory of their normally grown siblings. The aims of this study were to identify the nature, timing and possible causal factors influencing inadequate fetal growth in Large White × Landrace (LW) and Chinese Meishan (MS) gilts at three stages of pregnancy. Thirty-six per cent of litters contained inadequately grown fetuses. Both intrauterine-growth-restricted (IUGR) and small-for-gestational-age (SGA) fetuses could be identified as early as Day 30 in MS and LW litters and the percentage of litters containing inadequately grown fetuses was similar throughout gestation. MS fetuses, placentas and piglets had less within-litter variation in weight at all stages studied. Inverse relationships were observed between litter size and both minimum and mean weights of MS neonates. No other relationships between fetal size and either uterine position or litter size were observed.


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