Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects ...Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects may be carried over to the next generation or beyond. This phenomenon of the transgenerational impacts is known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences(namely, epigenetics). The mechanisms responsible for the epigenetic regulation of protein expression and functions include chromatin remodeling; DNA methylation(occurring at the 5′-position of cytosine residues within CpG dinucleotides); and histone modifications(acetylation, methylation, phosphorylation, and ubiquitination). Like maternal malnutrition, undernutrition during the neonatal period also reduces growth performance and feed efficiency(weight gain:feed intake; also known as weightgain efficiency) in postweaning pigs by 5–10%, thereby increasing the days necessary to reach the market bodyweight. Supplementing functional amino acids(e.g., arginine and glutamine) and vitamins(e.g., folate) play a key role in activating the mammalian target of rapamycin signaling and regulating the provision of methyl donors for DNA and protein methylation. Therefore, these nutrients are beneficial for the dietary treatment of metabolic disorders in offspring with intrauterine growth restriction or neonatal malnutrition. The mechanism-based strategies hold great promise for the improvement of the efficiency of pork production and the sustainability of the global swine industry.展开更多
Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages...Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development,possibly even during intrauterine life.This suggests that PCOS is either genetically-transmittedor is due to epigenetic alterations that develop in the intrauterine microenvironment.Although familial cases support the role of genetic factors,no specific genetic pattern has been defined in PCOS.Several candidate genes have been implicated in its pathogenesis,but none can specifically be implicated in PCOS development.Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories.The first is the "thrifty" phenotype hypothesis,which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and,as a compensatory mechanism,insulin resistance.Additionally,an impaired nutritional environment can affect the methylation of some specific genes,which can also trigger PCOS.The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues,causing the PCOS phenotype to develop in adult life.This review aimed to examine the role of fetal programming in development of PCOS.展开更多
Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult di...Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, preeclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity.展开更多
Under-nutrition as well as over-nutrition during pregnancy has been associated with the development of adult diseases such as diabetes and obesity.Both epigenetic modifications and programming of the mitochondrial fun...Under-nutrition as well as over-nutrition during pregnancy has been associated with the development of adult diseases such as diabetes and obesity.Both epigenetic modifications and programming of the mitochondrial function have been recently proposed to explain how altered intrauterine metabolic environment may produce such a phenotype.This review aims to report data reported in several animal models of fetal malnutrition due to maternal low protein or low calorie diet,high fat diet as well as reduction in placental blood flow.We focus our overview on the β cell.We highlight that,notwithstanding early nutritional events,mitochondrial dysfunctions resulting from different alteration by diet or gender are programmed.This may explain the higher propensity to develop obesity and diabetes in later life.展开更多
It is widely known that maternal physical exercise is able to induce beneficial improvements in offspring cognition; however, the effects of paternal exercise have not been explored in detail. The present study was de...It is widely known that maternal physical exercise is able to induce beneficial improvements in offspring cognition; however, the effects of paternal exercise have not been explored in detail. The present study was designed to evaluate the impact of paternal physical exercise on memory and learning, neuroplasticity and DNA methylation levels in the hippocampus of male offspring. Adult male Wistar rats were divided into two groups: sedentary or exercised fathers. The paternal preconception exercise protocol consisted of treadmill running, 20 minutes daily, 5 consecutive days per week for 22 days, while the mothers were not trained. After mating, paternal sperm was collected for global DNA methylation analysis. At postnatal day 53, the offspring were euthanized, and the hippocampus was dissected to measure cell survival by 5-bromo-2′-deoxiuridine and to determine the expression of synaptophysin, reelin, brain-derived neurotrophic factor and global DNA methylation levels. To measure spatial memory and learning changes in offspring, the Morris water maze paradigm was used. There was an improvement in spatial learning, as well as a significant decrease in hippocampal global DNA methylation levels in the offspring from exercised fathers compared with those from sedentary ones; however, no changes were observed in neuroplasticity biomarkers brain-derived neurotrophic factor, reelin and 5-bromo-2′-deoxiuridine. Finally, the global DNA methylation of paternal sperm was not significantly changed by physical exercise. These results suggest a link between paternal preconception physical activity and cognitive benefit, which may be associated with hippocampal epigenetic programming in male offspring. However, the biological mechanisms of this modulation remain unclear.展开更多
Background:Maternal nutrition during gestation affects fetal development,which has long-term programming effects on offspring postnatal growth performance.With a critical role in protein and lipid metabolism,essential...Background:Maternal nutrition during gestation affects fetal development,which has long-term programming effects on offspring postnatal growth performance.With a critical role in protein and lipid metabolism,essential fatty acids can influence the development of muscle and adipose tissue.The experiment investigated the effects of late gestation supplements(77 d prepartum),either rich in saturated and monounsaturated fatty acids(CON;155 g/cow/d EnerGII)or polyunsaturated fatty acids(PUFA;80 g/cow/d Strata and 80 g/cow/d Prequel),on cow performance and subsequent calf growth performance as well as mRNA expression in longissimus muscle(LM)and subcutaneous adipose tissue at birth and weaning.Results:There was no difference(P≥0.34)in cow body weight(BW)or body condition score from presupplementation through weaning.Relative concentrations of C18:3n-3 and C20:4n-6 decreased(P≤0.05)to a greater extent from mid-supplementation to calving for PUFA compared with CON cows.Cow plasma C20:0,C20:5n-3,and C22:6n-3 were increased(P≤0.01)in PUFA during supplementation period.At birth,PUFA steers had greater(P=0.01)plasma C20:5n-3.No differences(P≥0.33)were detected in steer birth BW or dam milk production,however,CON steers tended(P=0.06)to have greater pre-weaning average daily gain and had greater(P=0.05)weaning BW compared with PUFA.For mRNA expression in steers:MYH7 and C/EBPβin LM increased(P≤0.04)to a greater extent from birth to weaning for PUFA compared with CON;MYF5 in LM and C/EBPβin adipose tissue tended(P≤0.08)to decrease more from birth to weaning for CON compared with PUFA;SCD in PUFA adipose tissue tended(P=0.08)to decrease to a greater extent from birth to weaning than CON.In addition,maternal PUFA supplementation tended(P=0.08)to decrease MYOG mRNA expression in LM and decreased(P=0.02)ZFP423 in adipose tissue during the pre-weaning stage.Conclusions:Late gestation PUFA supplementation decreased pre-weaning growth performance of the subsequent steer progeny compared with CON supplementation,which co展开更多
Background:Omega-3 PUFA or methionine(Met)supply during gestation alters offspring physiology.However,the effect of both nutrients on fetal development has not been explored.Our objective was to determine the effects ...Background:Omega-3 PUFA or methionine(Met)supply during gestation alters offspring physiology.However,the effect of both nutrients on fetal development has not been explored.Our objective was to determine the effects of supplementation of these two nutrients during late gestation on fetal growth,DNA methylation,and mRNA expression of genes associated with the inflammatory response,and DNA methylation.Ewes(n=5/treatment)were fed from day 100 to 145 of gestation one of the following treatments:1)basal diet(NS)without fatty acids(FS)or methionine(MS)supplementation;2)FS(10 g/kg Ca salts,source omega-3 PUFA);3)MS(1 g/kg rumen protected methionine);and 4)FS and MS(FS-MS).On day 145,ewes were euthanized,and data from dams and fetus was recorded.Placenta(cotyledon),fetal liver,and blood samples were collected.Results:A treatments interaction on fetal liver weight,ewe body weight and body condition score(BCS)was observed;FS-MS were heavier(P<0.01)than FS and MS,and FS-MS ewes had a better(P=0.02)BCS than NS.Methionine increased(P=0.03)ewe plasma glucose concentration.Fetal liver global DNA methylation increased(P<0.01)in FS and MS.Dietary treatments modify the mRNA relative expression on some of the genes evaluated.In the fetal liver,FS increased(P=0.04)the mRNA relative expression of arachidonate-5-lipoxygenase-activatingprotein and tended to decrease(P=0.06)methionine-adenosyltransferase-1A.Moreover,MS decreased(P=0.04)DNA-methyltransferase-1 and tended to decrease(P=0.08)free-fatty-acid-receptor-1 mRNA relative expression.Furthermore,FS-MS decreased mRNA relative expression of tumor-necrosis-factor-alpha(P=0.05),peroxisomeproliferator-activated-receptor-delta(P=0.03)and gamma(P=0.04),tended to decrease(P≤0.09)interleukin-6,fatty-acid-transport-protein-1,and delta-5-desaturase,and increased adenosylhomocysteinase(P=0.04)mRNA relative expression.In cotyledon,FS tended to decrease fatty acid binding protein 4(P=0.09)mRNA relative expression.Conclusion:Omega-3 PUFA and Met supplementation improves dam’s performance in展开更多
Over the past few decades,genetic selection and refined nutritional management have extensively been used to increase the growth rate and lean meat production of livestock.However,the rapid growth rates of modern bree...Over the past few decades,genetic selection and refined nutritional management have extensively been used to increase the growth rate and lean meat production of livestock.However,the rapid growth rates of modern breeds are often accompanied by a reduction in intramuscular fat deposition and increased occurrences of muscle abnor‑malities,impairing meat quality and processing functionality.Early stages of animal development set the long‑term growth trajectory of offspring.However,due to the seasonal reproductive cycles of ruminant livestock,gestational nutrient deficiencies caused by seasonal variations,frequent droughts,and unfavorable geological locations nega‑tively affect fetal development and their subsequent production efficiency and meat quality.Therefore,enrolling live‑stock in nutritional intervention strategies during gestation is effective for improving the body composition and meat quality of the offspring at harvest.These crucial early developmental stages include embryonic,fetal,and postnatal stages,which have stage‑specific effects on subsequent offspring development,body composition,and meat quality.This review summarizes contemporary research in the embryonic,fetal,and neonatal development,and the impacts of maternal nutrition on the early development and programming effects on the long‑term growth performance of livestock.Understanding the developmental and metabolic characteristics of skeletal muscle,adipose,and fibrotic tissues will facilitate the development of stage‑specific nutritional management strategies to optimize production efficiency and meat quality.展开更多
The concept “fetal programming” shows who still in the intrauterine life, can interfere in factors related to the genesis and development of diseases in childhood, adolescence and adult life. The literature shows th...The concept “fetal programming” shows who still in the intrauterine life, can interfere in factors related to the genesis and development of diseases in childhood, adolescence and adult life. The literature shows that children born to mothers with gestational diabetes mellitus (GDM) are at increased risk for the development of obesity in adulthood, it becomes fundamental to study more about the subject. Obesity is a disease of multifactorial etiology, resulting from complex interactions between genetic and environmental factors. However, the marked increase in its incidence, precocity and severity are not yet fully understood. Several findings suggest that stressor stimuli (e.g. diabetes, nutritional changes) during intrauterine development may promote epigenetic changes, as well as affect mitochondrial metabolism, which may modulate fetal development and predispose to the late development of diseases. Despite the considerable amount of evidence accumulated about intrauterine programming for diseases of adult life, the determinant mechanisms of such programming are not yet clear.展开更多
People born with low birth weight are at a greater risk of developing later life diseases such as hypertension, diabetes and cancer. Recent studies have pinpointed the placenta as a critical factor involved in develop...People born with low birth weight are at a greater risk of developing later life diseases such as hypertension, diabetes and cancer. Recent studies have pinpointed the placenta as a critical factor involved in developmental programming. Changes in maternal lifestyle or dietary habits can alter placental development and increase the risk of developmental programming of adult diseases. Saudi people, including pregnant women, change their lifestyle and eating habits during the holy month of Ramadan. Previous studies found that the exposure to Ramadan lifestyle reduces placental weight;however, effects on other placental aspects remained unknown. We aimed to further examine the effects of exposure to Ramadan lifestyle on full-term placental morphometrics, histology and gene expression of key glucose transporters. To examine this, fresh placentas were collected from 60 healthy Saudi women. Samples were equally classified into two groups;not exposed to Ramadan lifestyle (control) or exposed to Ramadan lifestyle in the first. Placental weight, length and breadth were recorded and placental surface area was calculated. Placental tissue was processed and stained with eosin and hematoxylin for histological examination. Apoptosis was assessed using TUNEL assay. The gene expression of the glucose transporters GLUT1 and GLUT3 was evaluated. The results show that women exposed to Ramadan lifestyle have more elongated placentas with less central cord insertion. Placental weight and surface area were significantly lowered in women exposed to Ramadan lifestyle. Placental length was not affected but the breadth was significantly smaller in than control. Placentas exposed to Ramadan lifestyle had fewer and less-developed syncytial knots and thicker syncytiotrophoblast cells. Apoptosis was detected in placentas exposed to Ramadan lifestyle. GLUT1 mRNA expression was unaltered, but GLUT3 was increased compared to control group. These findings suggest that changes in maternal lifestyle during Ramadan can alter placental structure at m展开更多
It is generally believed that genotype and adult lifestyle elements are primary risks of diabetes mellitus. However, increasing evidence demonstrates that early life malnutrition during the period of gestation and/or...It is generally believed that genotype and adult lifestyle elements are primary risks of diabetes mellitus. However, increasing evidence demonstrates that early life malnutrition during the period of gestation and/or lactation may increase our susceptibility to some metabolic diseases in later life and the underlying mechanism is not very clear. Recently, epigenetics is hypothesized to be the important molecular basis of the imbalanced early life nutrition and glucose metabolism disorders. The fundamental mechanism is that early developmental nutrition can regulate epigenetic modifications of some genes associated with development and metabolism. MicroRNAs （miRNAs） are recognized as an important epigenetic modification and they are a major class of small noncoding RNAs （about 20-22 nucleotides） which can mediate posttranscriptional regulation of target genes with cell differentiation and apoptosis. Recent studies suggest that miRNAs may be the crucial modulators of fetal epigenetic programming in nutrition and metabolic disorders. How miRNAs can modulate the relationship between early life nutrition and disease susceptibilities, especially for aberrant glucose metabolism？展开更多
基金supported by the National Basic Research Program of China(2013CB127302)the National Natural Science Foundation of China(31272450 and 31572412)+2 种基金Competitive Grants from the Animal Reproduction Program(no.2014-67015-21770)Animal Growth & Nutrient Utilization Programs(no.2015-67015-23276)of the USDA National Institute of Food and AgricultureTexas A&M AgriL ife Research(H-8200)
文摘Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects may be carried over to the next generation or beyond. This phenomenon of the transgenerational impacts is known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences(namely, epigenetics). The mechanisms responsible for the epigenetic regulation of protein expression and functions include chromatin remodeling; DNA methylation(occurring at the 5′-position of cytosine residues within CpG dinucleotides); and histone modifications(acetylation, methylation, phosphorylation, and ubiquitination). Like maternal malnutrition, undernutrition during the neonatal period also reduces growth performance and feed efficiency(weight gain:feed intake; also known as weightgain efficiency) in postweaning pigs by 5–10%, thereby increasing the days necessary to reach the market bodyweight. Supplementing functional amino acids(e.g., arginine and glutamine) and vitamins(e.g., folate) play a key role in activating the mammalian target of rapamycin signaling and regulating the provision of methyl donors for DNA and protein methylation. Therefore, these nutrients are beneficial for the dietary treatment of metabolic disorders in offspring with intrauterine growth restriction or neonatal malnutrition. The mechanism-based strategies hold great promise for the improvement of the efficiency of pork production and the sustainability of the global swine industry.
文摘Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development,possibly even during intrauterine life.This suggests that PCOS is either genetically-transmittedor is due to epigenetic alterations that develop in the intrauterine microenvironment.Although familial cases support the role of genetic factors,no specific genetic pattern has been defined in PCOS.Several candidate genes have been implicated in its pathogenesis,but none can specifically be implicated in PCOS development.Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories.The first is the "thrifty" phenotype hypothesis,which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and,as a compensatory mechanism,insulin resistance.Additionally,an impaired nutritional environment can affect the methylation of some specific genes,which can also trigger PCOS.The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues,causing the PCOS phenotype to develop in adult life.This review aimed to examine the role of fetal programming in development of PCOS.
文摘Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, preeclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity.
基金Supported by the European Commission (FOOD-CT-2005007036)the Parthenon Trust (London,UK)+1 种基金the Belgian Fonds National de la Recherche Scientifiquethe Belgian Fonds pour la Recherche dans l’Industrie et l’Agriculture
文摘Under-nutrition as well as over-nutrition during pregnancy has been associated with the development of adult diseases such as diabetes and obesity.Both epigenetic modifications and programming of the mitochondrial function have been recently proposed to explain how altered intrauterine metabolic environment may produce such a phenotype.This review aims to report data reported in several animal models of fetal malnutrition due to maternal low protein or low calorie diet,high fat diet as well as reduction in placental blood flow.We focus our overview on the β cell.We highlight that,notwithstanding early nutritional events,mitochondrial dysfunctions resulting from different alteration by diet or gender are programmed.This may explain the higher propensity to develop obesity and diabetes in later life.
文摘It is widely known that maternal physical exercise is able to induce beneficial improvements in offspring cognition; however, the effects of paternal exercise have not been explored in detail. The present study was designed to evaluate the impact of paternal physical exercise on memory and learning, neuroplasticity and DNA methylation levels in the hippocampus of male offspring. Adult male Wistar rats were divided into two groups: sedentary or exercised fathers. The paternal preconception exercise protocol consisted of treadmill running, 20 minutes daily, 5 consecutive days per week for 22 days, while the mothers were not trained. After mating, paternal sperm was collected for global DNA methylation analysis. At postnatal day 53, the offspring were euthanized, and the hippocampus was dissected to measure cell survival by 5-bromo-2′-deoxiuridine and to determine the expression of synaptophysin, reelin, brain-derived neurotrophic factor and global DNA methylation levels. To measure spatial memory and learning changes in offspring, the Morris water maze paradigm was used. There was an improvement in spatial learning, as well as a significant decrease in hippocampal global DNA methylation levels in the offspring from exercised fathers compared with those from sedentary ones; however, no changes were observed in neuroplasticity biomarkers brain-derived neurotrophic factor, reelin and 5-bromo-2′-deoxiuridine. Finally, the global DNA methylation of paternal sperm was not significantly changed by physical exercise. These results suggest a link between paternal preconception physical activity and cognitive benefit, which may be associated with hippocampal epigenetic programming in male offspring. However, the biological mechanisms of this modulation remain unclear.
文摘Background:Maternal nutrition during gestation affects fetal development,which has long-term programming effects on offspring postnatal growth performance.With a critical role in protein and lipid metabolism,essential fatty acids can influence the development of muscle and adipose tissue.The experiment investigated the effects of late gestation supplements(77 d prepartum),either rich in saturated and monounsaturated fatty acids(CON;155 g/cow/d EnerGII)or polyunsaturated fatty acids(PUFA;80 g/cow/d Strata and 80 g/cow/d Prequel),on cow performance and subsequent calf growth performance as well as mRNA expression in longissimus muscle(LM)and subcutaneous adipose tissue at birth and weaning.Results:There was no difference(P≥0.34)in cow body weight(BW)or body condition score from presupplementation through weaning.Relative concentrations of C18:3n-3 and C20:4n-6 decreased(P≤0.05)to a greater extent from mid-supplementation to calving for PUFA compared with CON cows.Cow plasma C20:0,C20:5n-3,and C22:6n-3 were increased(P≤0.01)in PUFA during supplementation period.At birth,PUFA steers had greater(P=0.01)plasma C20:5n-3.No differences(P≥0.33)were detected in steer birth BW or dam milk production,however,CON steers tended(P=0.06)to have greater pre-weaning average daily gain and had greater(P=0.05)weaning BW compared with PUFA.For mRNA expression in steers:MYH7 and C/EBPβin LM increased(P≤0.04)to a greater extent from birth to weaning for PUFA compared with CON;MYF5 in LM and C/EBPβin adipose tissue tended(P≤0.08)to decrease more from birth to weaning for CON compared with PUFA;SCD in PUFA adipose tissue tended(P=0.08)to decrease to a greater extent from birth to weaning than CON.In addition,maternal PUFA supplementation tended(P=0.08)to decrease MYOG mRNA expression in LM and decreased(P=0.02)ZFP423 in adipose tissue during the pre-weaning stage.Conclusions:Late gestation PUFA supplementation decreased pre-weaning growth performance of the subsequent steer progeny compared with CON supplementation,which co
文摘Background:Omega-3 PUFA or methionine(Met)supply during gestation alters offspring physiology.However,the effect of both nutrients on fetal development has not been explored.Our objective was to determine the effects of supplementation of these two nutrients during late gestation on fetal growth,DNA methylation,and mRNA expression of genes associated with the inflammatory response,and DNA methylation.Ewes(n=5/treatment)were fed from day 100 to 145 of gestation one of the following treatments:1)basal diet(NS)without fatty acids(FS)or methionine(MS)supplementation;2)FS(10 g/kg Ca salts,source omega-3 PUFA);3)MS(1 g/kg rumen protected methionine);and 4)FS and MS(FS-MS).On day 145,ewes were euthanized,and data from dams and fetus was recorded.Placenta(cotyledon),fetal liver,and blood samples were collected.Results:A treatments interaction on fetal liver weight,ewe body weight and body condition score(BCS)was observed;FS-MS were heavier(P<0.01)than FS and MS,and FS-MS ewes had a better(P=0.02)BCS than NS.Methionine increased(P=0.03)ewe plasma glucose concentration.Fetal liver global DNA methylation increased(P<0.01)in FS and MS.Dietary treatments modify the mRNA relative expression on some of the genes evaluated.In the fetal liver,FS increased(P=0.04)the mRNA relative expression of arachidonate-5-lipoxygenase-activatingprotein and tended to decrease(P=0.06)methionine-adenosyltransferase-1A.Moreover,MS decreased(P=0.04)DNA-methyltransferase-1 and tended to decrease(P=0.08)free-fatty-acid-receptor-1 mRNA relative expression.Furthermore,FS-MS decreased mRNA relative expression of tumor-necrosis-factor-alpha(P=0.05),peroxisomeproliferator-activated-receptor-delta(P=0.03)and gamma(P=0.04),tended to decrease(P≤0.09)interleukin-6,fatty-acid-transport-protein-1,and delta-5-desaturase,and increased adenosylhomocysteinase(P=0.04)mRNA relative expression.In cotyledon,FS tended to decrease fatty acid binding protein 4(P=0.09)mRNA relative expression.Conclusion:Omega-3 PUFA and Met supplementation improves dam’s performance in
基金supported by the Agriculture and Food Research Initiative Competitive Grants(No.2015-67015-23219 and 2016-68006-24634)from the USDA National Institute of Food and Agriculture.
文摘Over the past few decades,genetic selection and refined nutritional management have extensively been used to increase the growth rate and lean meat production of livestock.However,the rapid growth rates of modern breeds are often accompanied by a reduction in intramuscular fat deposition and increased occurrences of muscle abnor‑malities,impairing meat quality and processing functionality.Early stages of animal development set the long‑term growth trajectory of offspring.However,due to the seasonal reproductive cycles of ruminant livestock,gestational nutrient deficiencies caused by seasonal variations,frequent droughts,and unfavorable geological locations nega‑tively affect fetal development and their subsequent production efficiency and meat quality.Therefore,enrolling live‑stock in nutritional intervention strategies during gestation is effective for improving the body composition and meat quality of the offspring at harvest.These crucial early developmental stages include embryonic,fetal,and postnatal stages,which have stage‑specific effects on subsequent offspring development,body composition,and meat quality.This review summarizes contemporary research in the embryonic,fetal,and neonatal development,and the impacts of maternal nutrition on the early development and programming effects on the long‑term growth performance of livestock.Understanding the developmental and metabolic characteristics of skeletal muscle,adipose,and fibrotic tissues will facilitate the development of stage‑specific nutritional management strategies to optimize production efficiency and meat quality.
文摘The concept “fetal programming” shows who still in the intrauterine life, can interfere in factors related to the genesis and development of diseases in childhood, adolescence and adult life. The literature shows that children born to mothers with gestational diabetes mellitus (GDM) are at increased risk for the development of obesity in adulthood, it becomes fundamental to study more about the subject. Obesity is a disease of multifactorial etiology, resulting from complex interactions between genetic and environmental factors. However, the marked increase in its incidence, precocity and severity are not yet fully understood. Several findings suggest that stressor stimuli (e.g. diabetes, nutritional changes) during intrauterine development may promote epigenetic changes, as well as affect mitochondrial metabolism, which may modulate fetal development and predispose to the late development of diseases. Despite the considerable amount of evidence accumulated about intrauterine programming for diseases of adult life, the determinant mechanisms of such programming are not yet clear.
文摘People born with low birth weight are at a greater risk of developing later life diseases such as hypertension, diabetes and cancer. Recent studies have pinpointed the placenta as a critical factor involved in developmental programming. Changes in maternal lifestyle or dietary habits can alter placental development and increase the risk of developmental programming of adult diseases. Saudi people, including pregnant women, change their lifestyle and eating habits during the holy month of Ramadan. Previous studies found that the exposure to Ramadan lifestyle reduces placental weight;however, effects on other placental aspects remained unknown. We aimed to further examine the effects of exposure to Ramadan lifestyle on full-term placental morphometrics, histology and gene expression of key glucose transporters. To examine this, fresh placentas were collected from 60 healthy Saudi women. Samples were equally classified into two groups;not exposed to Ramadan lifestyle (control) or exposed to Ramadan lifestyle in the first. Placental weight, length and breadth were recorded and placental surface area was calculated. Placental tissue was processed and stained with eosin and hematoxylin for histological examination. Apoptosis was assessed using TUNEL assay. The gene expression of the glucose transporters GLUT1 and GLUT3 was evaluated. The results show that women exposed to Ramadan lifestyle have more elongated placentas with less central cord insertion. Placental weight and surface area were significantly lowered in women exposed to Ramadan lifestyle. Placental length was not affected but the breadth was significantly smaller in than control. Placentas exposed to Ramadan lifestyle had fewer and less-developed syncytial knots and thicker syncytiotrophoblast cells. Apoptosis was detected in placentas exposed to Ramadan lifestyle. GLUT1 mRNA expression was unaltered, but GLUT3 was increased compared to control group. These findings suggest that changes in maternal lifestyle during Ramadan can alter placental structure at m
文摘It is generally believed that genotype and adult lifestyle elements are primary risks of diabetes mellitus. However, increasing evidence demonstrates that early life malnutrition during the period of gestation and/or lactation may increase our susceptibility to some metabolic diseases in later life and the underlying mechanism is not very clear. Recently, epigenetics is hypothesized to be the important molecular basis of the imbalanced early life nutrition and glucose metabolism disorders. The fundamental mechanism is that early developmental nutrition can regulate epigenetic modifications of some genes associated with development and metabolism. MicroRNAs （miRNAs） are recognized as an important epigenetic modification and they are a major class of small noncoding RNAs （about 20-22 nucleotides） which can mediate posttranscriptional regulation of target genes with cell differentiation and apoptosis. Recent studies suggest that miRNAs may be the crucial modulators of fetal epigenetic programming in nutrition and metabolic disorders. How miRNAs can modulate the relationship between early life nutrition and disease susceptibilities, especially for aberrant glucose metabolism？
