989 resultados para female offspring


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Avaliamos o efeito do consumo materno de SDG (Diglicosídeo Secoisolariciresinol) e de óleo de Linhaça+SDG sobre parâmetros bioquímicos e hormonais das ratas e das proles machos e fêmeas na lactação. As ratas lactantes foram separadas em: controle (C), ração controle cuja proteína foi caseína; (SDG): ração C com 400mg de SDG/Kg de ração; OLSDG: ração C com 400mg de SDG/Kg de ração e 7% de óleo de linhaça. No 14 e 20 dias de lactação as ratas foram ordenhadas e no 21 dia foram sacrificadas por punção cardíaca. Leite e soro foram coletados para avaliação bioquímica e hormonal. Hormônios foram quantificados por radioimunoensaio. As proles machos e fêmeas foram sacrificadas aos 14 e 21 dias de idade. Os animais foram eviscerados para análise da composição corporal. Monitoramos a ingestão alimentar e a massa corporal (MC) durante o período experimental. As ratas SDG apresentaram maior gordura corporal (GC; +39%), enquanto as OLSDG menor conteúdo mineral (-20%) e trigliceridemia (TG) (-39%). As ratas SDG e OLSDG apresentaram hiperprolactinemia (+389% e 153%, respectivamente) sem alteração na concentração de estradiol. No 14 dia de lactação, o leite das ratas OLSDG apresentou menores teores de lactose(-17%) e de proteínas (-20%) e o das ratas SDG apenas menor teor de proteína (-21%). A partir do 13 dia de lactação tanto os machos quanto as fêmeas OLSDG apresentaram menor MC (-14%, -16%, respectivamente). No 14 dia de lactação os machos SDG e OLSDG apresentaram menor gordura corporal (-24%, -55%, respectivamente ) e a prole SDG maior massa de gordura visceral (+39%). Os machos SDG apresentaram maiores concentrações de TG (+105%) e hipoprolactinemia (-41%). Os machos OLSDG também apresentaram hipoprolactinemia (-41%). As fêmeas SDG e OLSDG apresentaram maior estradiol aos 14 dias (+86% e +176%) que se normalizou aos 21 dias, maior colesterolemia (+16%) e as SDG apresentaram maior trigliceridemia (+74%). Aos 21 dias os machos e as fêmeas SDG e OLSDG apresentaram menor trigliceridemia (-48%, -54%,42% e -59%, respectivamente). Os dois componentes principais da semente de linhaça produzem alterações bioquímicas e hormonais tanto nas mães, quanto nas proles, independente do sexo. Entretanto, as alterações observadas diferem entre mães e prole e de acordo com o gênero. Entre as alterações mais importantes ressaltamos a hiperprolactinemia materna que pode ser um dos motivos para a hipoprolactinemia da prole e a hipertrigliceridemia causada pela ingestão de SDG pelas mães.

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α.O objetivo deste estudo foi avaliar se a restrição alimentar materna durante a lactação altera a função ovariana da prole na puberdade e na vida adulta. No dia do nascimento da ninhada, as ratas foram separadas aleatoriamente nos seguintes grupos: (C) controle = dieta com 23% de proteína; (PER) restrição protéica calórica = dieta com 8% de proteína. Após o desmame, as proles tiveram livre acesso a dieta com 23% proteína e apenas os animais na fase diestro foram sacrificados com uma dose letal de pentobarbital aos 40 e 90 dias de idade. O sangue foi retirado por punção cardíaca e o soro armazendo para posterior dosagem dos níveis hormonais por radioimunoensaio. O ovário direito foi excisado, pesado e armazenado a 80C para subseqüente avaliação do receptor de androgênio (AR), das isoformas dos receptores de estrogênio (ERα, ERβ1 e ERβ2), do receptor do hormônio folículo estimulante (FSHR), do receptor do hormonio luteinizante (LHR), das isoformas dos receptores de leptina (Ob-R, Ob-Ra and Ob-Rb), e da enzima aromatase pela técnica de RT-PCR. O ovário esquerdo foi incluido em parafina, seccionado em cortes de 5 μm de espessura e processado por análise histológica de rotina, para classificação dos foliculos ovarianos. Na puberdade, o grupo PER apresentou um aumento significativo (p<0,05) no número dos folículos pré-antrais e antrais, enquanto o número de folículos primordiais, folículos de Graaf e corpo lúteo foram reduzidos significativamente (p<0,05). As concentrações sericas de estradiol (pg/ml) foram significativamente aumentadas (p<0,05). Houve aumento significativo na expressão do RNAm dos FSHR (p<0.05) e LHR (p<0.05), e diminuição significativa na expressão do RNAm dos AR (p<0.05), ERα (p<0.05), ERβ1 (p<0.05) e ERβ2 (p<0.05). Na vida adulta, a restrição alimentar causou uma diminuição no número total de folículos ovarianos, entretanto esta redução só foi significativa no número dos folículos primordiais, primários e de Graaf (p<0.05). Houve redução significativa da expressão da enzima aromatase (p<0.01), do FSHR (p<0.05), LHR (p<0.05), Ob-R (p<0.05) e Ob-Rb (p<0.05). Podemos concluir que a restrição alimentar materna durante a lactação causa uma programação metabólica no ovário da prole, alterando a foliculogênese, expressão das diferentes isoformas dos receptores de estrogênio, leptina, androgênio e gonadotropinas e da enzima aromatase. Essa programação, possivelmente decorrente dos baixos níveis de leptina nos primeiros dias de vida, pode contribuir para uma senescência precoce e redução da fertilidade já descrita na literatura.

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Neosalanx taihuensis were sampled from the Tian-e-zhou Oxbow from March 2006 through November 2007. Two separate spawning seasons were identified based on the annual reproductive cycles of the females, designated as the autumn-spawning season and the spring-spawning season. Lifespan of the offspring of the spring-spawning fish was 1 year, with them dying after the subsequent spring spawning. Autumn-spawned females seem to be the offspring of the spring-spawning fish, based on monthly changes in the length-frequency distributions. Spring-mature females had higher absolute fecundity, gonadosomatic index, and relative condition factor in 2007 than in 2006. Relative condition factor of the immature female offspring of spring-spawning fish was higher in 2007 than in 2006, portending a further increase in reproductive investment during the spring spawning of 2008. The increasing reproductive investment suggests that the population of N. taihuensis in the Tian-e-zhou Oxbow may be recovering from its recent decline.

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Chinese rare minnow (Gobiocypris rarus), a freshwater teleost,. was exposed to diethylstilbestrol (DES) at 0.05, 0.5, 1 and 5 mug/L from fertilized eggs for up to mature period under flow-through condition. Several endpoints that related to development, reproductive fitness and transgenerational effects were evaluated. It was found that body length and body weight were significantly reduced and vitellogenin (Via) levels were significantly increased for fish exposed to DES. Histological examination showed that the sex ratios of F-0 fish skewed to female and about 2% of the fish exposed to 0.05 mug/L DES developed testes-ova. The reproductive success, as determined from data on egg production, was reduced in female fish exposed to 0.05, 0.5, 1 and 5 mug/L DES. The lowest-observed-effect concentrations (LOEC) for chances of sex ratios, reproductive success and histology alteration of F-0 are 0.05 mug/L. In the offspring, transgenerational effects on egg hatching rate. egg fertilization and Vtg levels of juvenile individuals were not observed. However. survival of F, generation fry significantly declined. The analysis of sex steroid levels revealed a significant decrease of testosterone (T) in the whole body homogenates (WBH) of male progeny and somewhat elevation of estradiol (E-T) in the WBH of female offspring. These findings indicate that exposure to DES causes a variety of developmental, reproductive and transgenerational effects. (C) 2004 Elsevier B.V. All rights reserved.

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A polyploid hybrid fish with natural gynogenesis can prevent segregation and maintain their hybrid vigor in their progenies. Supposing the reproduction mode of induced polyploid fish being natural gynogenesis, allopolyploid hybrid between common carp and crucian carp into allopolyploid was performed. The purpose of this paper is to describe a lineage from sexual diploid carp transforming into allotriploid and allotetraploid unisexual clones by genome addition. The diploid hybrid between common carp and crucian carp reproduces an unreduced nucleus consisting of two parental genomes. This unreduced female pronucleus will fuse with male pronucleus and form allotriploid zygote after penetration of related species sperms. Allotriploid embryos grow normally, and part of female allotriploid can produce unreduced mature ova with three genomes. Mature ova of most allotriploid females are provided with natural gynogenetic trait and their nuclei do not fuse with any entrance sperm. All female offspring are produced by gynogenesis of allotriploid egg under activation of penetrating sperms. These offspring maintain morphological traits of their allotriploid maternal and form an allotetraploid unisexual clone by gynogenetic reproduction mode. However, female nuclei of rare allotriploid female can fuse with penetrating male pronuclei and result in the appearance of allotetraploid individuals by means of genome addition. All allotetraploid females can reproduce unreduced mature eggs containing four genomes. Therefore, mature eggs of allotetraploid maintain gynogenetic trait and allotetraploid unisexual clone is produced under activation of related species sperms.

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Polycystic Ovary Syndrome (PCOS) is a complex disorder encompassing reproductive and metabolic dysfunction. Ovarian hyperandrogenism is an endocrine hallmark of human PCOS. In animal models, PCOS-like abnormalities can be recreated by in utero over-exposure to androgenic steroid hormones. This thesis investigated pancreatic and adrenal development and function in a unique model of PCOS. Fetal sheep were directly exposed (day 62 and day 82 of gestation) to steroidal excesses - androgen excess (testosterone propionate - TP), estrogen excess (diethylstilbestrol - DES) or glucocorticoid excess (dexamethasone - DEX). At d90 gestation there was elevated expression of genes involved in β- cell development and function: PDX-1 (P<0.001), and INS (P<0.05), INSR (P<0.05) driven by androgenic excess only in the female fetal pancreas. β- cell numbers (P<0.001) and in vitro insulin secretion (P<0.05) were also elevated in androgen exposed female fetuses. There was a significant increase in insulin secreting β-cell numbers (P<0.001) and in vivo insulin secretion (glucose stimulated) (P<0.01) in adult female offspring, specifically associated with prenatal androgen excess. At d90 gestation, female fetal adrenal gene expression was perturbed by fetal estrogenic exposure. Male fetal adrenal gene expression was altered more dramatically by fetal glucocorticoid exposure. In female adult offspring from androgen exposed pregnancies there was increased adrenal steroidogenic gene expression and in vivo testosterone secretion (P<0.01). This highlights that the adrenal glands may contribute towards excess androgen secretion in PCOS, but such effects might be secondary to other metabolic alterations driven by prenatal androgen exposure, such as excess insulin secretion Thus there may be dialogue between the pancreas and adrenal gland, programmed during early life, with implications for adult health Given both hyperinsulinaemia and hyperandrogenism are common features in PCOS, we suggest that their origins may be at least partially due to altered fetal steroidal environments, specifically excess androgenic stimulation

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Research into the evolutionary origins of sociality in insect colonies is changing emphasis from understanding how eusociality is maintained to how insects transition from solitary to social lifestyles. The pygmy carpenter bees (Ceratina spp.) offer an excellent model for investigating such factors as they have been historically thought of as solitary but have recently been shown to be socially polymorphic, which may indicate that they are currently in a transitive phase. By utilizing behavioural observation and experimental removal protocols, I show that extended parental care, as well as sibling care in Ceratina calcarata plays an important role in offspring development. I found, upon removal of the mother, that specifically produced ‘dwarf’ female offspring take over parental care roles in the nest. The existence of alloparental care and generational overlap suggests that although they are classified as solitary bees, C. calcarata possess the prerequisite behavioural repertoire for sociality.

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UNE EXPOSITION NÉONATALE À L’OXYGÈNE MÈNE À DES MODIFICATIONS DE LA FONCTION MITOCHONDRIALE CHEZ LE RAT ADULTE Introduction: L’exposition à l’oxygène (O2) des ratons nouveau-nés a des conséquences à l’âge adulte dont une hypertension artérielle (HTA), une dysfonction vasculaire, une néphropénie et des indices de stress oxydant. En considérant que les reins sont encore en développement actif lors des premiers jours après la naissance chez les rats, jouent un rôle clé dans le développement de l’hypertension et qu’une dysfonction mitochondriale est associé à une augmentation du stress oxydant, nous postulons que les conditions délétères néonatales peuvent avoir un impact significatif au niveau rénal sur la modulation de l’expression de protéines clés du fonctionnement mitochondrial et une production mitochondriale excessive d’espèces réactives de l’ O2. Méthodes: Des ratons Sprague-Dawley sont exposés à 80% d’O2 (H) ou 21% O2 (Ctrl) du 3e au 10e jr de vie. En considérant que plusieurs organes des rats sont encore en développement actif à la naissance, ces rongeurs sont un modèle reconnu pour étudier les complications d’une hyperoxie néonatale, comme celles liées à une naissance prématurée chez l’homme. À 4 et à 16 semaines, les reins sont prélevés et les mitochondries sont extraites suivant une méthode d’extraction standard, avec un tampon contenant du sucrose 0.32 M et différentes centrifugations. L’expression des protéines mitochondriales a été mesurée par Western blot, tandis que la production d’ H202 et les activités des enzymes clés du cycle de Krebs ont été évaluées par spectrophotométrie. Les résultats sont exprimés par la moyenne ± SD. Résultats: Les rats mâles H de 16 semaines (n=6) présentent une activité de citrate synthase (considéré standard interne de l’expression protéique et de l’abondance mitochondriales) augmentée (12.4 ± 8.4 vs 4.1 ± 0.5 μmole/mL/min), une diminution de l’activité d’aconitase (enzyme sensible au redox mitochondrial) (0.11 ± 0.05 vs 0.20 ± 0.04 μmoles/min/mg mitochondrie), ainsi qu’une augmentation dans la production de H202 (7.0 ± 1.3 vs 5.4 ± 0.8 ρmoles/mg protéines mitochondriales) comparativement au groupe Ctrl (n=6 mâles et 4 femelles). Le groupe H (vs Ctrl) présente également une diminution dans l’expression de peroxiredoxin-3 (Prx3) (H 0.61±0.06 vs. Ctrl 0.78±0.02 unité relative, -23%; p<0.05), une protéine impliquée dans l’élimination d’ H202, de l’expression du cytochrome C oxidase (Complexe IV) (H 1.02±0.04 vs. Ctrl 1.20±0.02 unité relative, -15%; p<0.05), une protéine de la chaine de respiration mitochondriale, tandis que l’expression de la protéine de découplage (uncoupling protein)-2 (UCP2), impliquée dans la dispersion du gradient proton, est significativement augmentée (H 1.05±0.02 vs. Ctrl 0.90±0.03 unité relative, +17%; p<0.05). Les femelles H (n=6) (vs Ctrl, n=6) de 16 semaines démontrent une augmentation significative de l’activité de l’aconitase (0.33±0.03 vs 0.17±0.02 μmoles/min/mg mitochondrie), de l’expression de l’ATP synthase sous unité β (H 0.73±0.02 vs. Ctrl 0.59±0.02 unité relative, +25%; p<0.05) et de l’expression de MnSOD (H 0.89±0.02 vs. Ctrl 0.74±0.03 unité relative, +20%; p<0.05) (superoxide dismutase mitochondriale, important antioxidant), tandis que l’expression de Prx3 est significativement réduite (H 1.1±0.07 vs. Ctrl 0.85±0.01 unité relative, -24%; p<0.05). À 4 semaines, les mâles H (vs Ctrl) présentent une augmentation significative de l’expression de Prx3 (H 0.72±0.03 vs. Ctrl 0.56±0.04 unité relative, +31%; p<0.05) et les femelles présentent une augmentation significative de l’expression d’UCP2 (H 1.22±0.05 vs. Ctrl 1.03±0.04 unité relative, +18%; p<0.05) et de l’expression de MnSOD (H 1.36±0.01 vs. 1.19±0.06 unité relative, +14%; p<0.05). Conclusions: Une exposition néonatale à l’O2 chez le rat adulte mène à des indices de dysfonction mitochondriale dans les reins adultes, associée à une augmentation dans la production d’espèces réactives de l’oxygène, suggérant que ces modifications mitochondriales pourraient jouer un rôle dans l’hypertension artérielle et d’un stress oxydant, et par conséquent, être un facteur possible dans la progression vers des maladies cardiovasculaires. Mots-clés: Mitochondries, Reins, Hypertension, Oxygène, Stress Oxydant, Programmation

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1. Fig trees (Ficus) are pollinated only by agaonid wasps, whose larvae also gall fig ovules. Each ovule develops into either a seed (when pollinated) or a wasp (when an egg is also laid inside) but not both. 2. Ovipositing wasps (foundresses) favour ovules near the centre of the enclosed inflorescence (syconium or 'fig'), leaving ovules near the outer wall to develop into seeds. This spatial stratification of wasps and seeds ensures reproduction in both partners, and thereby enables mutualism persistence. However, the mechanism(s) responsible remain(s) unknown. 3. Theory shows that foundresses will search for increasingly rare inner ovules and ignore outer ovules, as long as ovipositing in outer ovules is sufficiently slow and/or if inner ovules confer greater fitness to wasps. The fig-pollinator mutualism can therefore be stabilized by strong time constraints on foundresses and by offspring fitness gradients over variation in ovule position. 4. Female fig wasps cannot leave their galls without male assistance. We found that females in outer ovules were unlikely to be released. Inner ovules thus have added value to foundresses, because their female offspring are more likely to mate and disperse. 5. For those offspring that did emerge, gall position (inner/outer) and body size did not influence the order in which female pollinators exited syconia, nor did early emerging wasps enjoy increased life spans. 6. We also found that the life spans of female wasps nearly doubled when given access to moisture. We suggest that conflict resolution in the fig-pollinator mutualism may thus be influenced by tropical seasonality, because wasps may be less able to over-exploit ovules in dry periods due to time constraints.

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Prenatal testosterone excess leads to neuroendocrine, ovarian, and metabolic disruptions, culminating in reproductive phenotypes mimicking that of women with polycystic ovary syndrome (PCOS). The objective of this study was to determine the consequences of prenatal testosterone treatment on periovulatory hormonal dynamics and ovulatory outcomes. To generate prenatal testosterone-treated females, pregnant sheep were injected intramuscularly (days 30-90 of gestation, term = 147 days) with 100 mg of testosterone-propionate in cottonseed oil semi-weekly. Female offspring born to untreated control females and prenatal testosterone-treated females were then studied during their first two breeding seasons. Sheep were given two injections of prostaglandin F-2alpha 11 days apart, and blood samples were collected at 2-h intervals for 120 h, 10-min intervals for 8 h during the luteal phase (first breeding season only), and daily for an additional 15 days to characterize changes in reproductive hormonal dynamics. During the first breeding season, prenatal testosterone-treated females manifested disruptions in the timing and magnitude of primary gonadotropin surges, luteal defects, and reduced responsiveness to progesterone negative feedback. Disruptions in the periovulatory sequence of events during the second breeding season included: 1) delayed but increased preovulatory estradiol rise, 2) delayed and severely reduced primary gonadotropin surge in prenatal testosterone-treated females having an LH surge, 3) tendency for an amplified secondary FSH surge and a shift in the relative balance of FSH regulatory proteins, and 4) luteal responses that ranged from normal to anovulatory. These outcomes are likely to be of relevance to developmental origin of infertility disorders and suggest that differences in fetal exposure or fetal susceptibility to testosterone may account for the variability in reproductive phenotypes.

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There is strong evidence from animal studies that prenatal stress has different effects on male and female offspring. In general, although not always, prenatal stress increases anxiety, depression and stress responses, both hypothalamic–pituitary–adrenal and cardiovascular, in female offspring rather than in male. Males are more likely to show learning and memory deficits. There have been few studies so far in humans which differentiate effects of prenatal stress on male and female psychopathology. Some studies support the animal models, but the evidence is inconsistent. The mediating mechanisms for any sex specific effects are little understood, but there is evidence that placental function can differ depending on the sex of the fetus. We suggest that there may be an evolutionary reason for any sex differences in the long term effects of prenatal stress. In a stressful environment it may be adaptive for females, who are more likely to stay in one place and look after children, to be more vigilant, alert to danger and thus show more stress responsiveness. This can give rise to a more anxious or depressed phenotype. With males it may be more adaptive to go out and explore new environments, compete with other males, and be more aggressive. For this it may help to be less responsive to external stressors. More research is needed into sex differences in the effects of prenatal stress in humans, to test these ideas.

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Uteroplacental insufficiency has been shown to impair insulin action and glucose homeostasis in adult offspring and may act in part via altered mitochondrial biogenesis and lipid balance in skeletal muscle. Bilateral uterine vessel ligation to induce uteroplacental insufficiency in offspring (Restricted) or sham surgery was performed on day 18 of gestation in rats. To match the litter size of Restricted offspring, a separate cohort of sham litters had litter size reduced to five at birth (Reduced Litter), which also restricted postnatal growth. Remaining litters from sham mothers were unaltered (Control). Offspring were studied at 6 mo of age. In males, both Restricted and Reduced Litter offspring had reduced gastrocnemius PPAR γ coactivator-1α (PGC-1 α) mRNA and protein, and mitochondrial transcription factor A (mtTFA) and cytochrome oxidase (COX) III mRNA (P < 0.05), whereas only Restricted had reduced skeletal muscle COX IV mRNA and protein and glycogen (P < 0.05), despite unaltered glucose tolerance, homeostasis model assessment (HOMA) and intramuscular triglycerides. In females, only gastrocnemius mtTFA mRNA was lower in Reduced Litter offspring (P < 0.05). Furthermore, glucose tolerance was not altered in any female offspring, although HOMA and intramuscular triglycerides increased in Restricted offspring (P < 0.05). It is concluded that restriction of growth due to uteroplacental insufficiency alters skeletal muscle mitochondrial biogenesis and metabolic characteristics, such as glycogen and lipid levels, in a sex-specific manner in the adult rat in the absence of impaired glucose tolerance. Furthermore, an adverse postnatal environment induced by reducing litter size also restricts growth and alters skeletal muscle mitochondrial biogenesis and metabolic characteristics in the adult rat.

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There is a strong inverse relationship between a females own birth weight and her subsequent risk for gestational diabetes with increased risk of developing diabetes later in life. We have shown that growth restricted females develop loss of glucose tolerance during late pregnancy with normal pancreatic function. 


The aim of this study was to determine whether growth restricted females develop long-term impairment of metabolic control after an adverse pregnancy adaptation. Uteroplacental insufficiency was induced by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) in late pregnancy (E18) in F0 female rats. F1 Control and Restricted female offspring were mated with normal males and allowed to deliver (termed Ex-Pregnant). Age-matched Control and Restricted Virgins were also studied and glucose tolerance and insulin secretion were determined. Pancreatic morphology and hepatic glycogen and triacylglycerol content were quantified respectively.

Restricted females were born lighter than Control and remained lighter at all time points studied (p<0.05). Glucose tolerance, first phase insulin secretion and liver glycogen and triacylglycerol content were not different across groups, with no changes in β-cell mass. Second phase insulin secretion was reduced in Restricted Virgins (-34%, p<0.05) compared to Control Virgins, suggestive of enhanced peripheral insulin sensitivity but this was lost after pregnancy. Growth restriction was associated with enhanced basal hepatic insulin sensitivity, which may provide compensatory benefits to prevent adverse metabolic outcomes often associated with being born small. A prior pregnancy was associated with reduced hepatic insulin sensitivity with effects more pronounced in Controls than Restricted.

Our data suggests that pregnancy ameliorates the enhanced peripheral insulin sensitivity in growth restricted females and has deleterious effects for hepatic insulin sensitivity, regardless of maternal birth weight.

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Growth restriction impacts on offspring development and increases their risk of disease in adulthood which is exacerbated with "second hits." The aim of this study was to investigate if blood pressure, glucose tolerance, and skeletal muscle mitochondrial biogenesis were altered in 12-month-old male and female offspring with prenatal or postnatal growth restriction. Bilateral uterine vessel ligation induced uteroplacental insufficiency and growth restriction in offspring (Restricted). A sham surgery was also performed during pregnancy (Control) and some litters from sham mothers had their litter size reduced (Reduced litter), which restricted postnatal growth. Growth-restricted females only developed hypertension at 12 months, which was not observed in males. In Restricted females only homeostasis model assessment for insulin resistance was decreased, indicating enhanced hepatic insulin sensitivity, which was not observed in males. Plasma leptin was increased only in the Reduced males at 12 months compared to Control and Restricted males, which was not observed in females. Compared to Controls, leptin, ghrelin, and adiponectin were unaltered in the Restricted males and females, suggesting that at 12 months of age the reduction in body weight in the Restricted offspring is not a consequence of circulating adipokines. Skeletal muscle PGC-1α levels were unaltered in 12-month-old male and female rats, which indicate improvements in lean muscle mass by 12 months of age. In summary, sex strongly impacts the cardiometabolic effects of growth restriction in 12-month-old rats and it is females who are at particular risk of developing long-term hypertension following growth restriction.

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This study aimed to evaluate the performance and profitability of Canindé goats kept under semi-intensive management in mix farming system. 84 animals were used, being 81 does e three bucks.. The means of fertility rate at parturition, prolificacy and percentages of pregnant, kid survival and reproductive rate were compared by Tukey test at significance level of 5.0%. The kid weights from birth to weaning were submitted to variance analysis considering sex and birth type and the means were compared by Tukey test at 5.0% of significance. The percentages of fertility rate by ultrassographic were 91.36 and parturition 74.84. The prolificacy was 1.53. Independently of sex the mortality rate of kids from birth to weaning was 12.3. The average weights of offspring were 2.11 and 1.92 kg and 6.74 and 6.84 kg for male and female offspring at birth and weaning, in this order. The average weights of kids, meaning PN, P28, P56, P63, in the first season of kidding were 2.11 ± 0.46 kg, 3.63 ± 1.04 kg, 5.96 ± 158 kg and 6.74 ± 1.79 kg. There was significant differences (P<0,05) only to birth weight of kids sons of buck 135. However, the fertility at parturition for first and second breeding seasons (BS) were 87.65 and 62.96, respectively (P<0.05). The prolificacy was 1.58 and 1.47 to first and second BS in this order. The percentages of offspring survival from birth to weaning, to first and second BS were 92.86 and 80.00, respectively. From the first BS the reproduction rate was 1.28 while in the second was 0.74. After weaning the duration of lactation was 104 days to first breeding parturition and 38 days in the second one. The total milk production was 853.50 kg. The kids weight gain was influenced by season of year, wet and dry and buck (P<0.05). Were concluded that the seasons of year when breeding season and parturition occur strongly affected the productive performance and profitability of production system