989 resultados para female offspring
Retracted: Experimental evidence that maternal corticosterone controls adaptive offspring sex ratios
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1. Sex allocation theory has received considerable attention, yet the mechanism(s) by which mothers skew offspring sex ratios remain unknown. In birds, females are the heterogametic sex, which potentially gives them control of whether gametes will be male or female. How females might control the sex of the gamete is unclear, but one possibility is that variation in steroid hormones may mediate this process. 2. We experimentally altered circulating levels of corticosterone in female Gouldian finches (Erythrura gouldiae), a species that demonstrates both extreme stress responses and extreme offspring sex ratio biases when breeding with a low-quality (genetically incompatible) partner. 3. During egg production, individual females received both corticosterone and metyrapone (a corticosterone-synthesis inhibitor) implants, in random order, to induce both high and low levels of circulating stress hormones (within physiological limits). 4. We found that females with elevated corticosterone levels produced male-biased sex ratios, but when the same females were treated with metyrapone they produced female-biased offspring sex ratios. 5. These stress responses are adaptive because females constrained to breeding with low-quality males can substantially increase their fitness by overproducing sons. Changes in maternal corticosterone levels during stressful situations, such as the quality of a breeding partner, may provide an endocrine mechanism that can be exploited for strategic sex allocation.
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1.Sex allocation theory has received considerable attention, yet the mechanism(s) by which mothers skew offspring sex ratios remain unknown. In birds, females are the heterogametic sex, which potentially gives them control of whether gametes will be male or female. How females might control the sex of the gamete is unclear, but one possibility is that variation in steroid hormones may mediate this process. 2.We experimentally altered circulating levels of corticosterone in female Gouldian finches (Erythrura gouldiae), a species that demonstrates both extreme stress responses and extreme offspring sex ratio biases when breeding with a low-quality (genetically incompatible) partner. 3.During egg production, individual females received both corticosterone and metyrapone (a corticosterone-synthesis inhibitor) implants, in random order, to induce both high and low levels of circulating stress hormones (within physiological limits). 4.We found that females with elevated corticosterone levels produced male-biased sex ratios, but when the same females were treated with metyrapone they produced female-biased offspring sex ratios. 5.These stress responses are adaptive because females constrained to breeding with low-quality males can substantially increase their fitness by overproducing sons. Changes in maternal corticosterone levels during stressful situations, such as the quality of a breeding partner, may provide an endocrine mechanism that can be exploited for strategic sex allocation.
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Recent work suggests that rising spring temperatures over recent decades have eliminated many lizard populations, and threaten many more worldwide. However, because ambient temperatures constrain activity times in ectotherms, warming conditions (as expected under global climate change scenarios) can increase the duration of seasonal opportunities for courtship and mating. Thus, in species where polyandry results in enhanced offspring viability, a warming climate may not necessarily impair long-term survival. Our nine-year study of a sand lizard (Lacerta agilis) population near the northern range limit in Sweden revealed consistently higher incidence of multiple paternity of clutches in warmer years, and higher viability of offspring from multiply-sired clutches (presumably reflecting the advantages of more intense sperm competition). Any trend to warmer spring temperatures likely will benefit offspring viability in this system, by increasing a female's opportunities to mate with additional males.
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In rats, a maternal diet rich in lard is associated with reduced Na+,K+-ATPase activity in adult offspring kidney. We have addressed the role of different fatty acids by evaluating Na+,K+-ATPase activity in offspring of dams fed diets rich in saturated (SFA), monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids. Female Sprague–Dawley rats were fed, during pregnancy and suckling, a control diet (4% w/w corn oil) or a fatty acid supplemented diet (24% w/w). Offspring were reared on chow (4% PUFA) and studied at 6 months. mRNA expression (real-time PCR) of Na+,K+-ATPase α subunit and protein expression of Na+,K+-ATPase subunits (Western blot) were assessed in kidney and brain. Na+,K+-ATPase activity was reduced in kidney (P < 0.05 versus all groups) and brain (P < 0.05 versus control and MUFA offspring) of the SFA group. Neither Na+,K+-ATPase α1 subunit mRNA expression, nor protein expression of total α, α1, α2, α3 or β1 subunits were significantly altered in kidney in any dietary group. In brains of SFA offspring α1 mRNA expression (P < 0.05) was reduced compared with MUFA and PUFA offspring, but not controls. Also in brain, SFA offspring demonstrated reduced (P < 0.05) α1 subunit protein and increased phosphorylation (P < 0.05) of the Na+,K+-ATPase modulating protein phospholemman at serine residue 63 (S63 PLM). Na+,K+-ATPase activity was similar to controls in heart and liver. In utero and neonatal exposure to a maternal diet rich in saturated fatty acids is associated with altered activity and expression of Na+,K+-ATPase in adulthood, but mechanisms appear tissue specific.
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A suboptimal in utero environment leads to fetal adaptations to ensure short-term survival but in the long-term may lead to disease when the postnatal growth does not reflect that in utero. This study examined the effect of IUGR on whole body insulin sensitivity and metabolic activity in adult rats. Female Wistar-Kyoto rats were fed either a normal protein diet (NPD 20% casein) or a low protein diet (LPD; 8.7% casein) during pregnancy and 2 wk of lactation. In offspring at 32 wk of age, indirect calorimetry and dual energy x-ray absorptiometry (DEXA) were performed to assess metabolic activity and body composition. Insulin sensitivity was assessed using a euglycemic-hyperinsulinemic clamp. At 3 d of age, male and female LPD offspring were 23 and 27% smaller than controls, respectively. They remained significantly smaller throughout the experimental period (~10% smaller at 32 wk). Importantly, there was increased insulin sensitivity in LPD offspring (47% increase in males and 38% increase in females); pancreatic insulin content was normal. Body composition, O2 consumption, respiratory exchange ratio (RER), and locomotor activity were not different to controls. These findings suggest that in the absence of “catch-up” growth IUGR programs for improved insulin sensitivity.
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Children of obese mothers have increased risk of metabolic syndrome as adults. Here we report the effects of a high-fat diet in the absence of maternal obesity at conception on skeletal muscle metabolic and transcriptional profiles of adult male offspring. Female Sprague Dawley rats were fed a diet rich in saturated fat and sucrose [high-fat diet (HFD): 23.5% total fat, 9.83% saturated fat, 20% sucrose wt:wt] or a normal control diet [(CD) 7% total fat, 0.5% saturated fat, 10% sucrose wt:wt] for the 3 wk prior to mating and throughout pregnancy and lactation. Maternal weights were not different at conception; however, HFD-fed dams were 22% heavier than controls during pregnancy. On a normal diet, the male offspring of HFD-fed dams were not heavier than controls but demonstrated features of insulin resistance, including elevated plasma insulin concentration [40.1 ± 2.5 (CD) vs 56.2 ± 6.1 (HFD) mU/L; P = 0.023]. Next-generation mRNA sequencing was used to identify differentially expressed genes in the offspring soleus muscle, and gene set enrichment analysis (GSEA) was used to detect coordinated changes that are characteristic of a biological function. GSEA identified 15 upregulated pathways, including cytokine signaling (P < 0.005), starch and sucrose metabolism (P < 0.017), inflammatory response (P < 0.024), and cytokine-cytokine receptor interaction (P < 0.037). A further 8 pathways were downregulated, including oxidative phosphorylation (P < 0.004), mitochondrial matrix (P < 0.006), and electron transport/uncoupling (P < 0.022). Phosphorylation of the insulin signaling protein kinase B was reduced [2.86 ± 0.63 (CD) vs 1.02 ± 0.27 (HFD); P = 0.027] and mitochondrial complexes I, II, and V protein were downregulated by 50-68% (P < 0.005). On a normal diet, the male offspring of HFD-fed dams did not become obese adults but developed insulin resistance, with transcriptional evidence of muscle cytokine activation, inflammation, and mitochondrial dysfunction. These data indicate that maternal overnutrition, even in the absence of prepregnancy obesity, can promote metabolic dysregulation and predispose offspring to type 2 diabetes.
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Molting females of Monteiro's Hornbills (Tockus monteiri) seal themselves in nest cavities to breed until chicks are about half grown. To gain insight into the chronology of energy requirements of the Monteiro's Hornbill family unit in relation to this peculiar breeding strategy, we measured a number of ecological, physiological, and environmental variables during the Monteiro's Hornbill's breeding season. Those measurements included rates of energy expenditure of female Monteiro's Hornbills while in the nest cavity, characterizing their thermal environment, timing of egg laying, molt, hatching and fledging of chicks, as well as measuring clutch size and chick growth. Temperatures within the nest box varied between 12 and 39°C and did not affect the female energy expenditure. Female body mass and energy expenditure averaged 319 g and 5 W, respectively, at the start of concealment and decreased by on average 1.1 g day -1 and 0.05 W day -1 during at least the first 30 days of the 52-58 day concealment period. Clutch size varied between 1 and 8 and averaged 4.1 eggs, with eggs averaging only 66% of the mass predicted for a bird of this size. Over the range of chick ages at which the female might leave the nest, the predicted energy requirements for maintenance and tissue growth for a Monteiro's Hornbill chick increase sharply from 1.2 W at age 8 to 3.0 W at age 25. Reduction of the female energy requirement with time, the relatively low growth rate and therewith low energy requirements of Monteiro's Hornbill chicks, and an appropriate timing of the female's exodus from the nest cavity all aid in containing peak energy demands to levels that are sustainable for the food provisioning male.
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Polyandry is an important component of both sexual selection and kin structuring within cooperatively breeding species. A female may have multiple partners within a single reproductive attempt (simultaneous polyandry) or across multiple broods within and/or across years (sequential polyandry). Both types of polyandry confer a range of costs and benefits to individuals and alter the genetic structure of social groups over time. To date, many molecular studies of cooperative breeders have examined the evolution of cooperative breeding in relation to simultaneous polyandry. However, cooperatively breeding vertebrates are iteroparous, and thus sequential polyandry is also likely, but more rarely considered in this context. We examined sequential polyandry in a cooperatively breeding bird that has a low level of within-brood polyandry. Over a 5-year period (2006–2010), we monitored individual mating relationships using molecular markers in a population of individually marked apostlebirds (Struthidea cinerea). Divorce occurred between reproductive seasons in 17 % (8/48) of pairs and appeared to be female-driven. The level of sequential polyandry was also driven by the disappearance of males after breeding, and over 90 % of females, for whom we had suitable data, bred with multiple males over the period of study. This sequential polyandry significantly altered the relatedness of group members to the offspring in the nest. However, in about half of the cases, the second male was related (first- or second-order relative) to the first male of a sequentially polyandrous female and this alleviated the reduction in relatedness caused by polyandry. Our findings suggest that even in species with high within-brood parentage certainty, helper-offspring relatedness values can quickly erode through sequential polyandry.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Background and objective: Stress during pregnancy may alter offspring susceptibility to diseases during adulthood. In the present study, female Lewis rats were subjected to chronic stress during the gestational period, and the effect of this stress was evaluated histometrically on the progression of ligature-induced bone loss in their adult offspring.Material and methods: After confirming pregnancy, half of the pregnant rats were randomly designated as control animals (no stress regimen was imposed), and the other half was submitted to a chronic stress model (immobilization at cold temperature) between the 7th and the 18th gestational day. After birth, 12 male rats delivered by stressed mothers - Group 1 (G1) - and 12 male rats delivered by non-stressed mothers - Group 2 (G2) - were selected. When birthed rats reached 250 g of body weight, a silk ligature was placed around their maxillary right second molar in order to induce bone loss. The non-ligated left side served as a control. Sixty days later, these animals were sacrificed by anaesthetic overdose. After routine laboratorial processing, images of the histological sections were digitized and submitted for histometric measurement using two parameters: histological attachment loss and bone loss.Results: on the ligated side, G1 presented with greater histological attachment and bone loss than G2 (p < 0.05). on the non-ligated control side, neither of the groups presented with alterations in these parameters (p > 0.05).Conclusion: The chronic stress regimen imposed on pregnant rats produced a greater progression of ligature-induced bone loss in their adult offspring. (C) 0 2011 Elsevier Ltd. All rights reserved.
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Background: Periodontal disease during pregnancy has been recognized as one of the causes of preterm and lowbirth- weight (PLBW) babies. Several studies have demonstrated that PLBW babies are prone to developing insulin resistance as adults. Although there is controversy over the association between periodontal disease and PLBW, the phenomenon known as programming can translate any stimulus or aggression experienced during intrauterine growth into physiologic and metabolic alterations in adulthood. The purpose of the present study is to investigate whether the offspring of rats with periodontal disease develop insulin resistance in adulthood. Methods: Ten female Wistar rats were divided into periodontal disease (PED) and control (CN) groups. All rats were mated at 7 days after induction of periodontal disease. Male offspring were divided into two groups: 1) periodontal disease offspring (PEDO; n = 24); and 2) control offspring (CNO; n = 24). Offspring body weight was measured from birth until 75 days. When the offspring reached 75 days old, the following parameters were measured: 1) plasma concentrations of glucose, insulin, fructosamine, lipase, amylase, and tumor necrosis factor-α (TNF-α); 2) insulin sensitivity (IS); and 3) insulin signal transduction (IST) in insulin-sensitive tissues. Results: Low birth weight was not detected in the PEDO group. However, plasma concentrations of glucose, insulin, fructosamine, lipase, amylase, and TNF-α were increased and IS and IST were reduced (P <0.05) in the PEDO group compared with the CNO group. Conclusion: Maternal periodontal disease may induce insulin resistance and reduce IST in adult offspring, but such alterations are not attributable to low birth weight.
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Studies have demonstrated that nutrient deficiency during pregnancy or in early postnatal life results in structural abnormalities in the offspring hippocampus and in cognitive impairment. In an attempt to analyze whether gestational protein restriction might induce learning and memory impairments associated with structural changes in the hippocampus, we carried out a detailed morphometric analysis of the hippocampus of male adult rats together with the behavioral characterization of these animals in the Morris water maze (MWM). Our results demonstrate that gestational protein restriction leads to a decrease in total basal dendritic length and in the number of intersections of CA3 pyramidal neurons whereas the cytoarchitecture of CA1 and dentate gyrus remained unchanged. Despite presenting significant structural rearrangements, we did not observe impairments in the MWM test. Considering the clear dissociation between the behavioral profile and the hippocampus neuronal changes, the functional significance of dendritic remodeling in fetal processing remains undisclosed. © 2012 ISDN.
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Exposure to environmental chemicals may contribute to reproductive disorders, especially when it occurs in critical periods of development. The female reproductive system can be a target for androgens derived from environmental contaminants or pathological conditions. The purpose of this study was to assess the long-term effects of androgens on uterine tissue after maternal exposure limited to the time of gestation and lactation. Pregnant Wistar rats were treated with testosterone propionate (TP) at 0.05. mg/kg, 0.1. mg/kg, 0.2. mg/kg or corn oil (vehicle), s.c., from gestational day 12 until the end of lactation. The results show changes in the pattern of expression of receptors for estrogen, progesterone, and androgen at all doses tested, and decreases in both apoptosis and cell proliferation indices at 0.1 and 0.2. mg/kg. We conclude that early TP exposure, under these experimental conditions, causes changes in cellular and molecular parameters that are essential for normal uterine function in the adult. © 2013 Elsevier Inc.