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Background: Docosahexaenoic acid (DHA) plays a crucial role in the growth and functional development of the infant brain. However, the impact of additional DHA supplementation on neurodevelopment in infants remains controversial in randomized controlled trials. In this systematic review and meta-analysis, we aimed to investigate the effects of prenatal and postnatal DHA supplementation on neurodevelopment. Methods: We systematically searched the MEDLINE, EMBASE, and Cochrane Library electronic databases using a predefined strategy until 8 February 2024. We extracted relevant study characteristics and outcomes related to the nervous system. Two independent reviewers critically evaluated the included studies to assess their validity and risk of bias. Results: A total of 21 studies met our inclusion criteria, one study was removed after quality assessment, and the meta-analysis included 9 randomized controlled trials. The meta-analysis results indicated that there was no statistically significant difference between the DHA supplementation group and the placebo group, as assessed by the Mental Development Index [MDI; mean difference (MD), 0.41; 95% confidence interval (CI), -0.91 to 1.73; p = 0.55]. However, the DHA group had a significantly higher Psychomotor Development Index (PDI) than the placebo group (MD, 1.47; 95% CI, 0.23 to 2.72; p = 0.02). Subgroup analyses based on populations showed that DHA supplementation was superior to placebo for infants in both MDI (language score conversion; MD, 2.05; 95% CI, -0.16 to 4.26; p = 0.07) and PDI (MD, 1.94; 95% CI, 0.23 to 3.65; p = 0.03). Other subgroup analyses indicated no statistical differences between the two groups. The remaining assessments that could not be summarized quantitatively underwent a narrative evaluation. Conclusion: Based on the BSID assessments, DHA supplementation in infants may have potential neurodevelopmental benefits. Because the meta-analysis included few high-quality articles and had some limitations, more relevant articles are needed to address the need for separate DHA supplementation in infants, pregnant women, and lactating mothers. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022348100, identifier: CRD42022348100.
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This study aims to reveal the mechanism of prenatal stress in affecting the testicular development of offspring rats and the intervention effects of Zuogui Pills via connexin 43(Cx43). Forty pregnant SD rats were randomized into a blank control group, a mo-del group, a high-dose(18.9 g·kg~(-1)) Zuogui Pills group, a low-dose(9.45 g·kg~(-1)) Zuogui Pills group, and a vitamin E(1.44 mg·kg~(-1)) group. The other groups except the blank control group was subjected to chronic unpredictable mild stress for the modeling of prenatal stress. The model was evaluated by sucrose preference test, open field test, and enzyme-linked immunosorbent assay(ELISA) of the glucocorticoid level. ELISA was employed to measure the thyroxine 4(T4), testosterone(T), and follicle-stimulating hormone(FSH) levels to assess kidney deficiency. Hematoxylin-eosin(HE) staining was employed to evaluate the status of testicular germ cells. An automatic sperm analyzer was used to measure the sperm quality. Immunofluorescence double staining was employed to detect the expression of Cx43 and follicle-stimulating hormone receptor(FSHR) in the testes of offspring rats. The mRNA and protein levels of Cx43, FSHR, phosphatidylinositol 3-kinase(PI3K), and protein kinase B(Akt) were determined by real-time fluorescence quantitative polymerase chain reaction and Western blot, respectively. Prenatal stress induced testicular development disorders in offspring rats. The HE staining results showed that on the day of birth, the model group had reduced seminiferous tubules in the testes, elevated FSH level in the serum, and lowered Cx43 level in the testicular tissue. Male offspring rats of 60 days old had reduced testicular spermatogenic function, decreased sperm quality, elevated FSH level and lowered T level in the serum, and down-regulated protein and mRNA levels of Cx43, FSHR, PI3K, and Akt in the testicular tissue. Zuogui Pills alleviated the abnormal development and dysfunction of testicles in the offspring rats caused by prenatal stress. In summary, Zuogui Pills may weaken the effects of prenatal stress on testicular development and spermatogenic function of offspring rats by activating the PI3K/Akt pathway to regulate Cx43 expression in the testicular tissue.
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Conexina 43 , Medicamentos de Ervas Chinesas , Proteínas Proto-Oncogênicas c-akt , Ratos , Masculino , Animais , Proteínas Proto-Oncogênicas c-akt/metabolismo , Conexina 43/genética , Conexina 43/metabolismo , Conexina 43/farmacologia , Ratos Sprague-Dawley , Fosfatidilinositol 3-Quinases/metabolismo , Sêmen/metabolismo , Testículo , Hormônio Foliculoestimulante/metabolismo , Hormônio Foliculoestimulante/farmacologia , RNA Mensageiro/metabolismoRESUMO
SCOPE: The disturbance of the hypothalamic-pituitary-gonadal (HPG) axis, gut microbiota (GM) community, and short-chain fatty acids (SCFAs) is a triggering factor for pubertal onset. The study investigates the effects of the long-term intake of aspartame on puberty and GM in animals and humans. METHODS AND RESULTS: Aspartame-fed female offspring rats result in vaginal opening time prolongation, serum estrogen reduction, and serum luteinizing hormone elevation. , 60 mg kg-1 aspartame treatment decreases the mRNA levels of gonadotropin-releasing hormone (GnRH), Kiss1, and G protein-coupled receptor 54 (GPR54), increases the mRNA level of RFamide-related peptide-3 (RFRP-3), and decreases the expression of GnRH neurons in the hypothalamus. Significant differences in relative bacterial abundance at the genus levels and decreased fecal SCFA levels are noted by 60 mg kg-1 aspartame treatment. Among which, Escherichia-Shigella is negatively correlated with several SCFAs. In girls, high-dose aspartame consumption decreases the risk of precocious puberty. CONCLUSIONS: Aspartame reduces the chance of puberty occurring earlier than usual in female offspring and girls. Particularly, 60 mg kg-1 aspartame-fed female offspring delays pubertal onset through the dysregulation of HPG axis and GM composition by inhibiting the Kiss1/GPR54 system and inducing the RFRP-3. An acceptable dose of aspartame should be recommended during childhood.
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Kisspeptinas , Puberdade Tardia , Humanos , Ratos , Feminino , Animais , Kisspeptinas/metabolismo , Kisspeptinas/farmacologia , Aspartame/efeitos adversos , Aspartame/metabolismo , Puberdade Tardia/metabolismo , Ratos Sprague-Dawley , Maturidade Sexual/fisiologia , Hormônio Liberador de Gonadotropina/genética , Hipotálamo/metabolismo , Puberdade , RNA Mensageiro/metabolismoRESUMO
Retrospective analyses were performed on a dataset of 1188 fall-calving, Brangus cow-calf pairs. Analyses 1 sorted cows according to their initial body condition score (BCS < 5 vs. ≥ 5) and whether they received (SUP) or not (NOSUP) prepartum supplementation of protein and energy. Analyses 2 sorted cows according to their calving BCS (BCS < 5 or ≥ 5) and BCS change from calving until the start of the breeding season (lost, maintained, or gained). Cows were not estrus synchronized and were assigned to natural breeding for 90 days. Prepartum supplementation increased (P = 0.04) pregnancy percentage in cows with initial BCS < 5 but not (P = 0.20) with initial BCS ≥ 5. Calf weaning weight was greatest (P ≤ 0.04) for calves born from SUP cows with an initial BCS ≥ 5 and did not differ (P ≥ 0.56) among all remaining groups. Among cows with calving BCS < 5, pregnancy percentage were less (P = 0.05) for cows that lost vs. maintained/gained BCS. Postpartum BCS change did not (P ≥ 0.16) impact pregnancy percentage of cows calving at BCS ≥ 5. Calf weaning weight increased (P < 0.01) for cows calving with BCS ≥ 5 vs. < 5 and was not impacted (P = 0.47) by postpartum BCS change. Therefore, precalving supplementation improved reproduction of cows with BCS below optimal and weaning weight of calves born from cows with BCS above optimal, whereas calving BCS was the major factor affecting postpartum BCS change and cow reproductive performance.
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Dieta , Reprodução , Gravidez , Feminino , Bovinos , Animais , Dieta/veterinária , Estudos Retrospectivos , Parto , Ração Animal/análise , Suplementos Nutricionais , Peso CorporalRESUMO
Increasing evidence indicates that maternal exposure to oxidized soybean oil (OSO) causes damage to the mother and offspring. The antioxidant resveratrol (Res) has a variety of health benefits. However, the protective effect of Res on mitigating offspring damage after maternal exposure to OSO and its mechanism remains unclear. Therefore, this study aimed to investigate the effect of Res on hepatic fatty acid metabolism and the jejunal barrier in suckling piglets after maternal OSO exposure. A total of 18 sows in late gestation were randomly assigned to three treatments. The sows were fed with a fresh soybean oil (FSO) diet, an OSO diet, or the OSO diet supplemented with 300 mg/kg Res (OSO + Res), respectively. The results showed that maternal supplementation of Res restored the mRNA levels of genes related to fatty acid metabolism and increased the activities of catalase (CAT) and total superoxide dismutase (T-SOD) in suckling piglets' livers under the OSO challenge. Moreover, the OSO + Res group restored the mRNA levels of occludin and claudin 4 in suckling piglet jejunum compared with the results of the OSO challenges. In summary, supplementation with Res improves hepatic fatty acid metabolism and intestinal barrier function of suckling piglets after maternal OSO challenge during late gestation and lactation.
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Jejuno , Óleo de Soja , Animais , Gravidez , Feminino , Suínos , Resveratrol/farmacologia , Óleo de Soja/farmacologia , Dieta/veterinária , Suplementos Nutricionais/análise , Lactação , Ácidos Graxos/farmacologia , Fígado , RNA Mensageiro/genética , Ração Animal/análiseRESUMO
CONTEXT: Adequate maternal thyroid hormone is vital for fetal neurodevelopment. Abnormal thyroid function can cause developmental defects in offspring from spontaneous pregnancies; however, research in assisted reproduction is lacking. OBJECTIVES: This work aimed to investigate the association between thyroid disorders and offspring neurodevelopment from assisted reproduction. METHODS: In this prospective and longitudinal birth cohort study (Jiangsu, China), we included 729 women who had their thyroid function tested before an assisted reproductive technology cycle and delivered liveborn babies between November 2015 and June 2020. Maternal thyroid function was assessed by measuring thyroid antibodies, free thyroxine, and serum thyrotropin. The third edition Bayley Scales of Infant and Toddler Development screening test (Bayley-III screening test) was used to assess infant neurodevelopment. RESULTS: In multivariable-corrected linear regression analysis, infants of women with subclinical hypothyroidism (SCH) demonstrated a significantly lower receptive communication score (ß = -.63; 95% CI, -1.12 to -0.14; P = .013), with stratified analysis showing a significant association among female offspring (ß = -.87; 95% CI, -1.59 to -0.15; P = .018) but a null association among male offspring (ß = -.44; 95% CI, -1.03 to 0.15; P = .145). No significant differences were found in the assisted pregnancy population with normal thyroid function and positive antibodies according to the diagnostic cutoffs applied to normal pregnant women. CONCLUSION: SCH in assisted pregnancies correlates with lower communication scores in 1-year-olds, especially in girls. We recommend medication for SCH throughout, regardless of thyroid autoantibody status.
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Técnicas de Reprodução Assistida , Testes de Função Tireóidea , Glândula Tireoide , Humanos , Feminino , Estudos Prospectivos , Masculino , Gravidez , Adulto , Lactente , Glândula Tireoide/fisiologia , Desenvolvimento Infantil/fisiologia , Estudos Longitudinais , Recém-Nascido , Efeitos Tardios da Exposição Pré-Natal , Transtornos do Neurodesenvolvimento/etiologia , Transtornos do Neurodesenvolvimento/epidemiologia , Coorte de Nascimento , Hipotireoidismo/epidemiologia , Hipotireoidismo/sangue , China/epidemiologia , Complicações na Gravidez/epidemiologia , Pré-Escolar , Doenças da Glândula Tireoide/epidemiologia , Doenças da Glândula Tireoide/sangueRESUMO
BACKGROUND: The maternal diet during gestation and lactation affects the health of the offspring. Konjac glucomannan (KGM) is a significantly functional polysaccharide in food research, possessing both antioxidant and prebiotic properties. However, the mechanisms of how KGM regulates maternal nutrition remain insufficient and limited. This study aimed to investigate maternal supplementation with KGM during late gestation and lactation to benefit both maternal and offspring generations. RESULTS: Our findings indicate that KGM improves serum low density lipoprotein cholesterol (LDL-C) and antioxidant capacity. Furthermore, the KGM group displayed a significant increase in the feed intake-related hormones neuropeptide tyrosine (NPY), Ghrelin, and adenosine monophosphate-activated kinase (AMPK) levels. KGM modified the relative abundance of Clostridium, Candidatus Saccharimonas, unclassified Firmicutes, and unclassified Christensenellaceae in sow feces. Acetate, valerate, and isobutyrate were also improved in the feces of sows in the KGM group. These are potential target bacterial genera that may modulate the host's health. Furthermore, Spearman's correlation analysis unveiled significant correlations between the altered bacteria genus and feed intake-related hormones. More importantly, KGM reduced interleukin-6 (IL-6) levels in milk, further improved IL-10 levels, and reduced zonulin levels in the serum of offspring. CONCLUSION: In conclusion, maternal dietary supplementation with KGM during late gestation and lactation improves maternal nutritional status by modifying maternal microbial and increasing lactation feed intake, which benefits the anti-inflammatory capacity of the offspring serum. © 2024 Society of Chemical Industry.
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Antioxidantes , Lactação , Animais , Suínos , Feminino , Gravidez , Mananas/farmacologia , Mananas/química , Leite , Bactérias , Suplementos Nutricionais , HormôniosRESUMO
Prenatal exposure to methamphetamine (METH) is an issue of global concern due to its adverse effects on offspring, particularly its impact on liver health, an area still not fully understood. Inulin, a recognized prebiotic, is thought to potentially ameliorate these developmental disorders and toxic injuries in progeny. To investigate the effects of prenatal METH exposure on the liver and the role of gut microbiota, we established a murine model, the subjects of which were exposed to METH prenatally and subsequently treated with inulin. Our findings indicate that prenatal METH exposure causes liver damage in offspring, as evidenced by a decreased liver index, histopathological changes, diminished glycogen synthesis, hepatic dysfunction, and alterations in mRNA profiles. Furthermore, it impairs the antioxidant system and induces oxidative stress, possibly due to changes in cecal microbiota and dysregulation of bile acid homeostasis. However, maternal inulin supplementation appears to restore the gut microbiota in offspring and mitigate the hepatotoxic effects induced by prenatal METH exposure. Our study provides definitive evidence of METH's transgenerational hepatotoxicity and suggests that maternal inulin supplementation could be an effective preventive strategy.
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Doença Hepática Induzida por Substâncias e Drogas , Microbioma Gastrointestinal , Metanfetamina , Efeitos Tardios da Exposição Pré-Natal , Gravidez , Feminino , Camundongos , Animais , Humanos , Metanfetamina/toxicidade , Inulina/farmacologia , Suplementos Nutricionais , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controleRESUMO
Mercury (Hg) is one of the major pollutants in the environment, which requires effective countermeasures to manage its risk to both human health and the ecosystem. The antagonistic effect of selenium (Se) against methyl mercury (MeHg) and HgCl2 was evaluated using parent and offspring Caenorhabditis elegans (C. elegans) in this study. Through designated acute exposure of 24 h, our results showed that both MeHg and HgCl2 induced dose-dependent reproductive toxicity, including increased germ cell apoptosis, decrease in the number of oocytes, brood size, and sperm activation. The increased germ cell apoptosis was even higher in F1 and F2 generations, but returned to control level in F3 generation. Pretreatment with Se significantly suppressed the reproductive toxicity caused by Hg in both parental worms and their offspring, but had little influence on Hg accumulation. The protective role of Se was found closely related to the chemical forms of Hg: mtl-1 and mtl-2 genes participated in reducing the toxicity of HgCl2, while the gst-4 gene was involved in the reduced toxicity of MeHg. The formation of Se-Hg complex and the antioxidant function of Se were considered as possible antagonistic mechanisms. Our data indicated that pretreatment with Se could effectively protect C. elegans and their offspring against the reproductive toxicity of Hg in different chemical forms, which provided a reference for the prevention of Hg poisoning and essential information for better understanding the detoxification potential of Se on heavy metals.
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Mercúrio , Compostos de Metilmercúrio , Selênio , Animais , Humanos , Masculino , Mercúrio/toxicidade , Selênio/toxicidade , Caenorhabditis elegans/genética , Ecossistema , Sêmen , Compostos de Metilmercúrio/toxicidadeRESUMO
Bariatric surgery (BS) has emerged as an efficient approach for addressing obesity, offering long-term benefits encompassing substantial weight loss and improving metabolic disorders. Many women of childbearing age opt for BS to enhance their health and well-being. The weight loss achieved through these procedures can positively impact pregnancy outcomes, but it's crucial to consider potential drawbacks. Micronutrient deficiencies, such as anemia resulting from iron or vitamin B12 deficiency, are a legitimate concern. Making the decision to have a BS is a complex process with many possible obstacles. The complicated nature of this decision is highlighted by worries about dumping syndrome, surgical complications that could include the risk of internal hernias, and the possibility that infants could be labeled as small for gestational age because of maternal undernourishment. Furthermore, there is a notable absence of international consensus regarding the ideal timing for conceiving after undergoing BS. Therefore, this narrative review extensively explores the existing body of literature, offering insights into the prevailing challenges encountered before and during pregnancy following BS. These challenges encompass a wide range of considerations, commencing with fertility-related issues. The study will cover strategies for addressing vitamin and nutritional deficiencies through supplementation, subtleties of post-BS altered glucose metabolism and how it affects the detection and treatment of gestational diabetes, how dumping syndrome progresses, various surgical problems, and how different bariatric procedures affect pregnancy and fetal outcomes. These include a tendency to give birth to children considered undersized for gestational age, nutritional deficits, anemia, and abnormal maternal glucose metabolism. This review offers a comprehensive exploration of the multifaceted landscape of pregnancy in the context of BS. It aims to provide a valuable resource for healthcare professionals and women considering pregnancy after undergoing BS, enabling them to make well-informed decisions and receive appropriate care during this critical phase of life.
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BACKGROUND: The maternal diet is essential to offspring development, but the specific effects on tooth morphology are still unknown. The aim of this study was to evaluate the effects of altering maternal calcium (Ca) and phosphorus (P) supplementation during gestation and lactation on offspring dentition. METHODS: Pregnant mice were fed an experimental diet containing a threefold increase in Ca and a threefold decrease in P compared to the standard mouse chow diet at embryonic Day 0.5 (E0.5). Offspring mice were maintained on standard or experimental diets from post-natal Day 0 to weaning, then fed control diets until 6 weeks of age. Six-week-old offspring heads were collected and scanned using micro-computed tomography. Dental morphometrics of offspring maxillary and mandibular first and third molars (n = 5-6 per diet/per sex) were determined. A two-way ANOVA test was employed to verify the existence of any significant differences between groups. The significance level was set at P < .05. RESULTS: A two-way ANOVA revealed a statistically significant interaction between the effects of diet and sex on the upper and lower dentition. Moreover, experimental diet-fed female offspring exhibited smaller molars with shorter mesiodistal width and larger pulp chambers relative to controls, while experimental diet-fed male offspring possessed larger molars with wider mesiodistal width and smaller pulp chambers. CONCLUSION: Our findings reveal that altering the maternal and offspring dietary Ca:P ratio during gestation, lactation and weaning led to significant, sex-specific changes in the offspring dentition. The differences in dentition appeared to be correlated with the sex-specific changes in the craniofacial skeleton.
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This study aimed to explore the effects and mechanisms of maternal gestational diabetes mellitus (GDM) and selenium (Se) deficiency on the growth and glucose metabolism of offspring. Female C57BL/6J mice were divided into four groups as follows: a control group, a GDM group, a Se deficiency group, and a GDM with Se deficiency group. GDM animal models were established via S961. Pregnant mice fed their offspring until weaning. Then, offspring continued to be fed with a basic diet until adulthood. Body weight and fasting blood glucose were measured weekly. Se content, oxidative stress indicators, and the protein expression of the PI3K/Akt signaling pathway were detected. GDM increased susceptibility to obesity in lactating offspring, with gender differences observed in adult offspring. The effect of Se deficiency on SOD activity only appeared in female offspring during adulthood but was shown in male offspring during weaning though it disappeared during adulthood. GDM and Se deficiency increased the risk of abnormal glucose metabolism in female offspring from weaning to adulthood but gradually decreased in male offspring. The influence on the expression of PI3K/Akt signaling pathway-related proteins showed the same trend. GDM and Se deficiency affected the growth and glucose metabolism of offspring through oxidative stress and PI3K/Akt signaling pathway-related proteins, and gender differences existed.
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Diabetes Gestacional , Desnutrição , Selênio , Gravidez , Humanos , Masculino , Feminino , Animais , Camundongos , Glicemia/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Fosfatidilinositol 3-Quinases , Camundongos Endogâmicos C57BL , LactaçãoRESUMO
Maternal dietary patterns during pregnancy have been demonstrated to impact the structure of the gut microbiota in offspring, altering their susceptibility to diseases. This study is designed to elucidate whether the impact of folic acid supplementation during pregnancy on hepatic steatosis in male offspring of rat dams exposed to a high-fat diet (HFD) is related to gut-liver axis homeostasis. In this study, female rats were administered a HFD and simultaneously supplemented with 5 mg/kg folic acid throughout their pregnancy. Histopathological examination showed that folic acid supplementation effectively ameliorated hepatic lipid accumulation and inflammatory infiltrate in male offspring subjected to a maternal HFD. Maternal folic acid supplementation reduced the abundance of Desulfobacterota and the Firmicutes/Bacteroidota (F/B) ratio in male offspring. The expression of tight junction proteins in the colon was significantly upregulated, and the serum LPS level was significantly reduced. Furthermore, there was a notable reduction in the hepatic expression of the TLR4/NF-κB signaling pathway and subsequent inflammatory mediators. Spearman's correlation analysis revealed significant associations between hepatic inflammation-related indices and several gut microbiota, particularly Desulfobacterota and Lactobacillus. With a reduction in hepatic inflammation, the expression of PPAR-α was upregulated, and the expression of SREBP-1c and its downstream lipid metabolism-related genes was downregulated. In summary, folic acid supplementation during pregnancy modulates gut microbiota and enhances intestinal barrier integrity in male offspring of HFD dams. This helps reduce the LPS leakage and suppress the expression of TLR4/NF-κB pathway in the liver, thereby improving lipid metabolism disorders, and alleviating hepatic steatosis.
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Fígado Gorduroso , Microbioma Gastrointestinal , Gravidez , Ratos , Animais , Masculino , Feminino , Camundongos , Dieta Hiperlipídica/efeitos adversos , Lipopolissacarídeos/farmacologia , NF-kappa B/metabolismo , Receptor 4 Toll-Like/metabolismo , Fígado Gorduroso/prevenção & controle , Fígado Gorduroso/metabolismo , Fígado/metabolismo , Suplementos Nutricionais , Ácido Fólico/farmacologia , Ácido Fólico/metabolismo , Inflamação/metabolismo , Camundongos Endogâmicos C57BLRESUMO
At the end of gestation, fetal skeleton rapidly accumulates calcium, and bone development continues in offspring postnatally. To accommodate, maternal skeletal physiology is modulated in a serotonin-dependent manner. Selective serotonin reuptake inhibitors (SSRIs) are generally considered safe for treatment of major depressive disorder, postpartum depression, and other psychiatric illnesses during the peripartum period, but because serotonin affects bone remodeling, SSRIs are associated with decreased bone mass across all ages and sexes, and the impact of SSRIs during fetal and postnatal development has not been fully investigated. In the present study, our aim was to examine developmental fluoxetine exposure on offspring skeleton and to assess varying degrees of impact depending on dose and window of exposure in short-term and long-term contexts. We established that a low dose of lactational fluoxetine exposure caused a greater degree of insult to offspring bone than either a low dose during fetal and postpartum development or a high dose during lactation only in mice. We further discovered lasting impacts of developmental fluoxetine exposure, especially during lactation only, on adult bone and body composition. Herein, we provide evidence fluoxetine exposure during early development may have detrimental effects on the skeleton of offspring at weaning and into adulthood.
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Transtorno Depressivo Maior , Efeitos Tardios da Exposição Pré-Natal , Feminino , Camundongos , Animais , Humanos , Fluoxetina/toxicidade , Inibidores Seletivos de Recaptação de Serotonina/toxicidade , Transtorno Depressivo Maior/tratamento farmacológico , Serotonina , Osso e Ossos , Efeitos Tardios da Exposição Pré-Natal/tratamento farmacológicoRESUMO
Early life nutrition can reprogram development and exert long-term consequences on body weight regulation. In mice, maternal high-fat diet (HFD) during lactation predisposed male but not female offspring to diet-induced obesity when adult. Molecular and cellular changes in the hypothalamus at important time points are examined in the early postnatal life in relation to maternal diet and demonstrated sex-differential hypothalamic reprogramming. Maternal HFD in lactation decreased the neurotropic development of neurons formed at the embryo stage (e12.5) and impaired early postnatal neurogenesis in the hypothalamic regions of both males and females. Males show a larger increased ratio of Neuropeptide Y (NPY) to Pro-opiomelanocortin (POMC) neurons in early postnatal neurogenesis, in response to maternal HFD, setting an obese tone for male offspring. These data provide insights into the mechanisms by which hypothalamic reprograming by early life overnutrition contributes to the sex-dependent susceptibility to obesity in adult life in mice.
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Dieta Hiperlipídica , Obesidade , Feminino , Camundongos , Animais , Masculino , Dieta Hiperlipídica/efeitos adversos , Obesidade/etiologia , Hipotálamo , Peso Corporal , LactaçãoRESUMO
We conducted a follow up of the children in Mongolia whose mothers received one of the three doses of vitamin D (600, 2000, or 4000 IU daily) during pregnancy as part of the randomized, double-blind, clinical trial of vitamin D supplementation to determine their impact on child health to two years. In the parental trial, 119 pregnant women were assigned to 600 IU/day, 121 were assigned 2000 IU/day, and 120 were assigned 4000 IU/day starting at 12-16 weeks' gestation and continuing throughout pregnancy. At baseline, maternal serum 25(OH)D concentrations were similar across arms; 91 % were 50 nmol/l. As expected, there was a dose-response association between the amount of vitamin D consumed (600, 2000, or 4000 IU daily) and maternal 25(OH)D levels at the end of the intervention. Total 311 children of 311 mothers were followed for 2 years to evaluate health outcomes. We determined the child's health outcomes (rickets, respiratory disease [pneumonia, asthma], and diarrhea/vomiting) using a questionnaire and physical examination (3, 6, and 24 months of age). Low levels of mothers' serum 25(OH)D during pregnancy increased the risk of developing rickets, respiratory illness, and other diseases in children during the early childhood period. Rickets was diagnosed in 15.6 % of children of women who received 600 IU of vitamin D during pregnancy, which was higher than in other vitamin D groups. Children in the group whose mothers received low doses of vitamin D (600 IU/day) had a greater probability of developing respiratory diseases compared to the other groups: pneumonia was diagnosed in n = 36 (35.0 %) which was significantly higher than the group receiving vitamin D 4000 IU/day (n = 34 (31.5 %) p = 0.048). In the group whose pregnant mother consumed 600 IU/day of vitamin D, the risk of child pneumonia was â¼ 2 times higher than in the group who consumed 4000 IU/day (OR=1.99, 95 % CI: 1.01-3.90). The incidence of diarrhea and vomiting in children was 12.1 % lower in the 2000 IU/day group and 13.1 % lower in the 4000 IU/day group compared with the 600 IU/day group (p = 0.051). The offspring of pregnant women who regularly used vitamin D at doses above 600 IU/day had lower respiratory disease, rickets, and diarrheal risks at 2 years.
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Pneumonia , Raquitismo , Deficiência de Vitamina D , Humanos , Feminino , Criança , Pré-Escolar , Gravidez , Saúde da Criança , Suplementos Nutricionais , Vitamina D , Vitaminas , Método Duplo-Cego , Diarreia , Vômito , Avaliação de Resultados em Cuidados de Saúde , ColecalciferolRESUMO
INTRODUCTION: Vitamin D (VitD) has been shown to impact neurodevelopment. Studies have shown that higher 25-hydroxy-vitamin D (25(OH)D) concentrations (the indicator of vitD status) may be associated with better neurodevelopmental outcomes, although current data are conflicting. This study examined the relationship between total circulating 25(OH)D concentrations and neurodevelopmental outcomes in 3-5-year-old (3-5 yo) children. METHODS: In this study, pregnant women were randomized to receive 400 (standard dose), 2000, or 4000 IU vitD3/day. Offspring then underwent the Brigance Screen at 3-5 yo. The 25(OH)D concentration was measured at birth and 3-5 yo. Relationships between Brigance scores and 25(OH)D and Brigance scores and vitamin D binding protein (VDBP) genotype were examined. RESULTS: Higher 25(OH)D at the time of testing was associated with better overall performance on neurodevelopmental testing as measured by the Brigance quotient (B = 0.208, p = 0.049). Scores were then broken down into sub-scores. Children born to mothers in the 2000 IU/day group scored higher on the Brigance language component of the assessment versus the standard dose group (B = 4.667, p = 0.044). The group of children who had the Gc1f-1s or Gc1f-2 genotypes scored higher on the Brigance academic component (B = 9.993, p < 0.001) and lower on the Brigance language component versus the 1f1f genotype (B = -9.313, p < 0.001). Children with the Gc1s-1s, Gc1s-2, or Gc2-2 genotypes also scored lower than the Gc1f-1f genotype (B = -6.757, p = 0.003). CONCLUSION: These results suggest that higher 25(OH)D concentrations early in life and higher doses of maternal vitamin D supplementation during pregnancy may have a positive association with neurodevelopmental outcomes. This study also suggests that the VDBP genotype is associated with neurodevelopment and differentially affects various fields of neurodevelopment.
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Deficiência de Vitamina D , Vitamina D , Recém-Nascido , Humanos , Criança , Feminino , Gravidez , Pré-Escolar , Vitaminas , Genótipo , Suplementos Nutricionais , Proteína de Ligação a Vitamina D/genética , ColecalciferolRESUMO
Parent-offspring conflict over food allocation can be modeled using two theoretical frameworks: passive (scramble competition) and active choice (signaling) resolution models. However, differentiating between these models empirically can be challenging. One possibility involves investigating details of decision-making by feeding parents. Different nestling traits, related to competitive prowess or signaling cryptic condition, may interact additively or non-additively as predictors of parental feeding responses. To explore this, we experimentally created even-sized, small broods of pied flycatchers and manipulated nestling cryptic quality, independently of size, by vitamin E supplementation. We explored how interactions between nestling cryptic condition, size, signals, and spatial location predicted food allocation and prey-testing by parents. Parents created the potential for spatial scramble competition between nestlings by feeding from and to a narrow range of nest locations. Heavier supplemented nestlings grew faster and were more likely to access profitable nest locations. However, the most profitable locations were not more contested, and nestling turnover did not vary in relation to spatial predictability or food supply. Postural begging was only predicted by nestling hunger and body mass, but parents did not favor heavier nestlings. This suggests that size-mediated and spatial competition in experimental broods was mild. Pied flycatcher fathers allocated food in response to nestling position and begging order, while mothers seemingly followed an active choice mechanism involving assessment of more complex traits, including postural intensity interacting with order, position, and treatment, and perhaps other stimuli when performing prey-testings. Differences in time constraints may underlie sex differences in food allocation rules.
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The oxidation of fats and oils is an undisputed subject of science, given the effect of oxidized fats and oils on food quality and safety. This study aimed to determine whether maternal exposure to oxidized soybean oil (OSO) causes lipid metabolism disorders in the liver and whether this lipid metabolism disorder can be transmitted to offspring or even worsened. A total of 60 female Sprague-Dawley (SD) rats were divided randomly into four groups in this study. Treatment groups received a pure diet of OSO with a peroxide value of 200, 400, or 800 mEqO2/kg, while the control group received fresh soybean oil (FSO). As for our results, OSO affected serum biochemical parameters in the maternal generation (F0) and induced liver histopathology changes, inflammation, and oxidative stress. Moreover, the expression of genes related to the liver X receptor α (LXRα)âsterol regulatory element binding protein-1c (SREBP-1c) signaling pathway was changed. Similar trends were found in the livers of offspring on postnatal days 21 and 56. In conclusion, exposure to OSO during gestation and lactation can affect liver lipid synthesis. Additionally, it is detrimental to the development of the offspring's liver, affecting fatty acid metabolism and causing liver damage.
Assuntos
Fígado , Óleo de Soja , Feminino , Ratos , Animais , Ratos Sprague-Dawley , Metabolismo dos Lipídeos , Ácidos GraxosRESUMO
Background: Vitamin D deficiency during pregnancy is common, but whether maternal vitamin D status affects glycolipid metabolism of offspring remains unclear. Objective: To evaluate the effect of maternal vitamin D deficiency during pregnancy on the glycolipid metabolism of offspring at different life-cycles (from birth to adulthood) and to explore the improvement of different dosages of vitamin D supplementation. Methods: Sprague-Dawley rats were fed vitamin D-deprived (VDD group) or standard vitamin D diets (SC group) during pregnancy, and their diets were changed to standard vitamin D diets during lactation (the offspring were sorted into VDDoffspring and SCoffspring groups). After weaning, rats in the VDDoffspring group were randomly assigned to the VDDoffspring, VDDoffspring-S3300 and VDDoffspring-S10000 groups with diets containing standard, medium and high dosages of vitamin D for 12 wk. Serum was collected for biochemical analyses at postnatal Day 21, postnatal Day 56 and postnatal Day 84. Oral glucose tolerance test (OGTT) was performed at postnatal Day 70. Results: Compared to SCoffspring, rats in the VDDoffspring group had significantly lower birth weight with faster weight gain and higher levels of lipid metabolism in early life. After near adulthood, the differences in weight and lipid metabolism between the two groups disappeared. OGTT showed significantly higher blood glucose levels in the VDDoffspring group at 30 min, 60 min, and 90 min. The continuation of vitamin D supplementation at medium and high dosages after weaning did not cause any obvious changes in weight or glycolipid metabolism (except for postprandial hyperglycemia). OGTT demonstrated that the glucose levels in the VDDoffspring-S3300 group were lowest at all the time points and that those in the VDDoffspring-S10000 group were the highest at 30 min, 60 min, and 90 min among the three groups. Conclusion: The adverse effects of vitamin D deficiency during pregnancy on glycolipid metabolism in offspring vary in different stages. Over a long time period, adequate vitamin D supplementation is beneficial to glycolipid metabolism for the offspring of subjects with vitamin D deficiency during pregnancy; however, further improvement is required.