Journal of Developmental Origins of Health and Disease最新文献

{"title":"Intrauterine growth restriction promotes hypothalamic circadian dysregulation in adult mouse offspring.","authors":"Alexandra E O'Brien, Peter J Mark, Jeremy T Smith, Kimberley C W Wang","doi":"10.1017/S2040174425100214","DOIUrl":"https://doi.org/10.1017/S2040174425100214","url":null,"abstract":"<p><p>Adverse prenatal conditions can induce intrauterine growth restriction (IUGR) and increase the risk of adulthood metabolic disease. Mechanisms underlying developmentally programmed metabolic disease remain unclear but may involve disrupted postnatal circadian rhythms and kisspeptin signalling. We investigated the impact of maternal hypoxia-induced IUGR on hypothalamic and hepatic expression of clock genes (<i>Bmal1</i>, <i>Per2</i> and <i>Reverbα</i>), metabolic genes (<i>Pparα</i>, <i>Pparγ</i> and <i>Pgc1α</i>) and kisspeptin genes (<i>Kiss1</i> and <i>Kiss1r</i>) in adult offspring. Pregnant BALB/c mice were housed in hypoxic conditions (10.5% oxygen) from gestational day 11 to 17.5 and then returned to normoxic conditions until term (gestational day ∼ 21). Control animals were housed in normoxic conditions throughout pregnancy. Offspring were weighed at birth. At 8 weeks of age, body, liver and brain tissues were collected and weighed. Relative clock gene, metabolic gene and kisspeptin signalling gene expression were measured using qPCR. The IUGR offspring were lighter at birth and remained lighter at 8 weeks but with higher brain relative to body weight. The IUGR offspring had decreased hypothalamic <i>Bmal1</i> and <i>Reverbα</i> expression, but unchanged hepatic clock gene expression and no change in hypothalamic or hepatic <i>Per2</i> expression, compared with Control offspring. This tissue-specific change in clock gene expression suggests circadian dysregulation. There were no IUGR-related changes to metabolic gene expression in the hypothalamus or liver, but IUGR offspring had increased hypothalamic <i>Kiss1r</i> expression. These results demonstrate IUGR offspring from hypoxia pregnancies show central circadian misalignment and potentially disrupted hypothalamic <i>Kiss1/Kiss1r</i> signalling, which may contribute to developmentally programmed metabolic disease.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e36"},"PeriodicalIF":1.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the bifidogenic effect of various infant formula supplementations: a systematic review and network meta-analysis of randomized controlled trials.","authors":"Fatemeh Mansouri, Mahnaz Mardani, Maryam Rezapour, Laura Bordoni, Rosita Gabbianelli","doi":"10.1017/S2040174425100196","DOIUrl":"10.1017/S2040174425100196","url":null,"abstract":"<p><p>This study aimed to investigate the effects of infant formula supplements on <i>Bifidobacterium</i> level in the infant gut through a systematic review and network meta-analysis (NMA) of randomized controlled trials (RCTs).Systematic review included PubMed, EMBASE, MEDLINE, Scopus, Web of Science, and Cochrane CENTRAL to identify RCTs evaluating the effects of formulas supplemented with prebiotics, probiotics, synbiotics, β-palmitic acid, or combinations of β-palmitic acid with prebiotics on infant gut <i>Bifidobacterium</i> levels. A meta-analysis compared bifidogenic effects to standard formula. The main outcome was the relative abundance (RA) of <i>Bifidobacterium</i> in fecal samples measured by various microbiota assessment techniques, with effect sizes as mean differences and standard deviations. An overall effect estimate was derived using a random-effects model. NMA assessed formula effects using breastfeeding as the reference.Nineteen studies were included. Compared to standard formula, supplementation with prebiotics (<i>p</i> < 0.0001), synbiotics (<i>p</i> < 0.0001), β-palmitic acid (<i>p</i> = 0.0005), or β-palmitic acid combined with prebiotics (<i>p</i> < 0.0001) significantly increased <i>Bifidobacterium</i> levels in the infant gut. Probiotic supplementation showed no significant effect (<i>p</i> = 0.9755). NMA and p-score ranking, comparing formulas to breastmilk, indicated that prebiotic-supplemented formulas with the lowest ranking <i>p</i>-score (0.2764), most closely resembled breastfeeding's bifidogenic effect. However, prebiotics and probiotics were analyzed as broad categories, and group variability may affect outcomes. In conclusion, formula supplementation with prebiotics, synbiotics, β-palmitic acid, or combinations of β-palmitic acid with prebiotics increased the RA of <i>Bifidobacterium</i> in infant's gut, with prebiotic formula most closely mimicking the bifidogenic effects of breastfeeding.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e35"},"PeriodicalIF":1.5,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between low birth weight, childhood adversity, and natural disaster with delay discounting among children.","authors":"Shuhei Terada, Yuto Maeda, Pamela J Surkan, Takeo Fujiwara","doi":"10.1017/S2040174425100160","DOIUrl":"https://doi.org/10.1017/S2040174425100160","url":null,"abstract":"<p><p>According to the Developmental Origins of Health and Disease (DOHaD) hypothesis, low-birthweight (LBW) infants are programmed to seek additional resources as compensation for early deprivation. However, no study has yet explored this in the context of delay discounting (DD), which refers to the tendency to prefer smaller, immediate rewards over larger, delayed ones. Both prenatal factors, such as LBW, and postnatal factors, including adverse childhood experiences (ACEs) and exposure to natural disasters, may influence DD. To investigate whether LBW children seek larger future rewards, we analyzed LBW's effect on DD, accounting for ACEs and natural disaster exposure. This prospective cohort study involved 167 children from areas affected by the Great East Japan Earthquake (GEJE), with a mean age of 8.3 years at the time of the DD experiment. LBW was assessed in the 2012 baseline questionnaire using the Mother-Child Handbook, along with ACEs prior to the GEJE and traumatic earthquake experiences. In 2014, DD was assessed through a token-based experiment where children allocated tokens for either immediate rewards (one candy per token for \"now\") or delayed rewards (two candies per token for \"one month later\"). Our results showed that children with LBW and three or more ACEs exhibited lower DD, while traumatic earthquake experiences were not associated with DD. These findings suggest that children with LBW and multiple ACEs may develop adaptive strategies to seek more resources, indicating a responsive reward system to childhood adversity, even after exposure to a severe natural disaster.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e32"},"PeriodicalIF":1.5,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetically predicted maternal prepregnancy BMI increased risk of childhood intestinal malformation: evidence from a Mendelian randomization study.","authors":"Siqi Xie, Xiaojin Zhuang, Lan Liu, Yifan Fang, Bing Zhang","doi":"10.1017/S2040174425100184","DOIUrl":"https://doi.org/10.1017/S2040174425100184","url":null,"abstract":"<p><p>The study aimed to explore the causal effect of maternal prepregnancy body mass index (BMI) on congenital malformations of intestine (CMI). The genome-wide association data of BMI and CMI were obtained via the Mendelian randomization (MR) base platform. Single nucleotide polymorphisms (SNPs) significantly associated with BMI in females were identified and used as instrumental variables, and the causal relationship between BMI in females and CMI was examined using the bidirectional two-sample MR analyses research method. Three statistical methods including inverse-variance weighted (IVW) method, weighted median estimator, and MR-Egger regression were employed. A total of 36 SNPs significantly associated with BMI in females were identified in the study (<i>P</i> < 5 × 10⁻⁸; linkage disequilibrium r² < 0.001). Consistent association between BMI in females and CMI was observed when evaluated by different methods (IVW: odds ratio (OR) 0.364, 95% confidence interval (CI) 0.144–0.922; weighted median estimator: OR 0.395, 95% CI 0.096–1.619; MR-Egger Method: OR 0.244, 95% CI 0.020–2.974), which suggests that BMI in females is negatively associated with increased risk of CMI. The MR analysis provided the strong evidence to indicate that decreasing BMI in females might be causally associated with the risk of CMI.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e34"},"PeriodicalIF":1.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of perinatal exposure to an endocrine disruptor mixture on the renal microenvironment of aged male rat offspring: histopathological aspects.","authors":"Pedro Meira Dolfini, Karianne Delalibera Hinokuma, Gisele Alborghetti Nai, Anthony César de Souza Castilho, Leonardo de Oliveira Mendes","doi":"10.1017/S2040174425100172","DOIUrl":"https://doi.org/10.1017/S2040174425100172","url":null,"abstract":"<p><p>The developmental origins of health and disease hypothesis suggests that environmental exposures during critical developmental windows increase the risk of disease later in life. Among these, endocrine disruptors (EDs) are particularly concerning due to their ubiquitous presence. The kidneys are highly susceptible to EDs toxicity during the perinatal period; however, long-term effects of ED mixtures on renal structure in aging remain unclear. This study aimed to characterize the renal histoarchitecture of aged rats after perinatal exposure to an ED mixture. Pregnant Sprague-Dawley rats were assigned to two groups: Control (corn oil, 2 ml/kg) and ED Mix (32.11 mg/kg/day of 12 EDs, including phthalates, pesticides, UV filters, bisphenol A, and butylparaben, in corn oil). Exposure occurred from gestational day 7 to postnatal day 21. Offspring were euthanized at postnatal day 440. ED mixture exposure did not affect the organosomatic index. However, ED Mix offspring presented renal lesions, including necrosis and tubular fusion, with a trend toward increased pathological changes. Morphometric analysis revealed enlarged nuclei and increased nuclear perimeters in the cortex and medulla, along with altered cellular organization in glomerular and medullary regions. Collagen organization was disrupted, with increased fibrosis in cortical and medullary compartments and reduced collagen type I and III in glomeruli. These findings indicate that perinatal exposure to an ED mixture alters nuclear phenotype and promotes extracellular matrix remodeling in distinct renal compartments. Such changes suggest long-term impacts on renal structure and function, emphasizing the health risks associated with early-life exposure to complex ED mixtures.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e33"},"PeriodicalIF":1.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between women's weight gain during their infancy and being overweight or underweight in adulthood: a retrospective cohort study.","authors":"Yukari Kudo, Kohei Ogawa, Hiromitsu Azuma, Yuka Wada, Aikou Okamoto, Seiji Wada","doi":"10.1017/S2040174425100202","DOIUrl":"https://doi.org/10.1017/S2040174425100202","url":null,"abstract":"<p><p>This study aimed to explore the associations between weight gain during infancy with pre-pregnant body mass index (BMI) later in life, focusing on risks of being overweight or underweight. A retrospective cohort study was conducted using data from women (<i>n</i> = 1082) who visited the National Center for Child Health and Development between 2017 and 2021. The participants provided their Maternal and Child Health Handbook, which included records of their own birthweight and weight gain from birth to 1, 3, and 6 months. The infant weight gain was divided into quintiles. Multivariable logistic regression was used to assess the association of weight gain during infancy with pre-pregnant underweight (BMI < 18.5) and overweight (BMI ≥ 25) later in life, adjusting for potential confounders. The current study found that the largest weight gain category (5230-7700 g) by 6 months was associated with a decreased risk of \"pre-pregnant underweight,\" compared to the third weight gain category (4355-4730 g) by 6 months (OR, 0.40; 95% CI, 0.22-0.73). In contrast, no significant association was observed between weight gain category in infancy and being overweight in adulthood. In conclusion, greater weight gain during the first 6 months of life was associated with a reduced risk of \"adult underweight,\" without increasing the risk of being overweight.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e36"},"PeriodicalIF":1.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of (-)-epicatechin in cardiac hypertrophy of male rats obese by programing.","authors":"Leticia Orozco-Arguelles, Sergio De Los Santos, Ramón M Coral-Vázquez, Claudia Cecilia Vega-García, Elena Zambrano, Patricia Canto","doi":"10.1017/S204017442510010X","DOIUrl":"https://doi.org/10.1017/S204017442510010X","url":null,"abstract":"<p><p>The obesogenic maternal environment can lead to cardiac hypertrophy in the offspring. The aim of this study was to investigate whether (-)-epicatechin (Epi) modify the expression of genes related to pathological cardiac hypertrophy (CH), and its physiological pathway, in offspring obese by programing. Four groups of eight male offspring Wistar rats of 110 days were randomly selected to control groups [C and offspring of maternal obesity (MO)] or to Epi groups (C + Epi or MO + Epi). In heart tissue, we evaluated the size of the ventricular walls and cavities, presence of fibrosis, mRNA and protein of Myh6, Myh7, Anp, Bnp, Acta 1, Col1a1, Akt, and Mtor. We observed an increase of the heart weight/body ratio in groups treated with Epi. Only in MO group, heart area and its perimeter were increased, as well as <i>Myh7</i> and <i>Anp</i> mRNA. We found a significant decrease of fibrosis area in male offspring treatment with Epi. In Epi group <i>Anp</i> mRNA was decreased whilst Anp protein in MO group was increased; further, a decrease in Col1a1 protein was found in MO group. In conclusion, the maternal obesity activates pathological CH markers reactivating fetal cardiac genes involved in histological changes observed in cardiac tissue. Epi treatment decreased the <b>content of collagen area</b> and expression of some fetal cardiac genes participating in this pathway in offspring of maternal obesity.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e31"},"PeriodicalIF":1.5,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144790461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic imprinting due to small litter size mitigates insulin resistance through the interscapular brown adipose tissue activation in a high-sucrose diet model.","authors":"Isabela Jesus de Deus, Aline Rezende Ribeiro de Abreu, Miliane Martins de Andrade Fagundes, Juliana Letícia Silva, Gustavo Silveira Breguez, Ângela Antunes Silva, Érika Cristina da Silva Oliveira Siqueira, Cláudia Martins Carneiro, Daniela Caldeira Costa, Sílvia Paula-Gomes, Karina Barbosa de Queiroz","doi":"10.1017/S2040174425100123","DOIUrl":"https://doi.org/10.1017/S2040174425100123","url":null,"abstract":"<p><p>Metabolic imprinting refers to lasting metabolic changes from early-life environmental exposures, especially nutritional, that impact adult health and chronic disease risk. We investigated whether metabolic imprinting by small litter size (SL) activates interscapular brown adipose tissue (iBAT) and affects glucose and lipid metabolism, oxidative damage, and insulin resistance (IR) in young rats exposed to a high-sucrose diet (HSD) over eight weeks. Male Wistar rats (<i>n</i> = 48) were assigned to control (eight pups/ dam; CL) and small litter (four pups/ dam; SL) groups. Post-weaning (21 days), they were divided into four dietary groups: (i) standard diet (STD, chow diet) from CL, or (ii) SL; (iii) HSD (30% sucrose) from CL, or (iv) SL, for eight weeks. Afterward, animals were euthanized for analysis of iBAT and serum samples. HSD caused hypertrophy, IR, and oxidative damage in iBAT. However, the SL model attenuated HSD-induced IR by up-regulating p-AKT (Ser 473) and activating iBAT thermogenesis, resulting in decreased PGC1-α expression and up-regulating UCP1 expression, which contributed to iBAT hyperplasia. Additionally, SL reduced PKA activation and free fatty acid (FFA) release, decreasing the lipid oxidative damage observed in HSD-fed iBAT. These findings suggest that SL-induced metabolic imprinting enhances iBAT thermogenesis through p-AKT (Ser 473) and PGC1-α signaling, increases UCP1 expression, and reduces PKA substrates phosphorylation, decreasing FFA levels and oxidative damage following HSD exposure. While our results challenge the existing literature, we propose that the metabolic plasticity from the SL model allows rats to adapt to dietary variations and may protect against HSD-induced IR in adulthood.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e29"},"PeriodicalIF":1.5,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144776725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between maternal glycohemoglobin in pregnancy and adult offspring cognition: results from the Transgenerational Effects of Adult Morbidity (TEAM) Study.","authors":"Katherine Bowers, Kimberly Yolton, Patrick Catalano, Jane C Khoury","doi":"10.1017/S2040174425100081","DOIUrl":"10.1017/S2040174425100081","url":null,"abstract":"<p><p>Maternal diabetes, a common pregnancy complication, has long-term implications for both mother and offspring. While the developmental origins of metabolic health from prenatal diabetes exposure are well known, cognitive consequences in offspring are still being explored. The timing of hyperglycemia during pregnancy that most affects cognitive development and whether these effects persist into adulthood remains unclear. This study aimed to determine the association between trimester-specific hyperglycemia exposure and adult cognition in the offspring of women with pregestational diabetes. The Transgenerational Effect on Adult Morbidity (TEAM) Study evaluated health outcomes in young adult offspring of mothers with pregestational diabetes who participated in a Diabetes in Pregnancy Program Project Grant (PPG) at the University of Cincinnati (1978-1995). The TEAM Study visit (March 2018 - August 2022) included a comprehensive clinical examination and cognitive assessment (Wechsler Abbreviated Scale of Intelligence - II). Linear regression estimated the association between prenatal hyperglycemia and offspring's perceptual reasoning and verbal comprehension. The mean age at follow-up was 32.1 years. Hyperglycemia during pregnancy was inversely associated with cognitive measures, controlling for confounders including maternal education and pre-pregnancy obesity. Higher glycohemoglobin in the second and third trimesters was significantly linked to lower IQ scores, matrix reasoning, and vocabulary subtest scores. Third-trimester hyperglycemia was also associated with lower block design subtest scores. In summary, hyperglycemia, particularly in the latter half of pregnancy, was associated with lower cognitive ability in adult offspring of women with pre-pregnancy pregestational diabetes.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e26"},"PeriodicalIF":1.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fetal programming under maternal heat stress: a focus on skeletal muscle growth and nutrition in livestock.","authors":"Weicheng Zhao, Rosa I Luna Ramirez, Robert P Rhoads, Laura D Brown, Sean W Limesand","doi":"10.1017/S2040174425100111","DOIUrl":"10.1017/S2040174425100111","url":null,"abstract":"<p><p>An adverse <i>in utero</i> experience negatively impacts perinatal growth in livestock. Maternal heat stress (HS) during gestation reduces placental growth and function. This progressive placental insufficiency ultimately leads to fetal growth restriction (FGR). Studies in chronically catheterized fetal sheep have shown that FGR fetuses exhibit hypoxemia, hypoglycemia, and lower anabolic hormone concentrations. Under hypoxic stress and nutrient deficiency, fetuses prioritize basal metabolic requirements over tissue accretion to support survival. Skeletal muscle is particularly vulnerable to HS-induced placental insufficiency due to its high energy demands and large contribution to total body mass. In FGR fetuses, skeletal muscle growth is reduced, evidenced by smaller myofiber size and mass, reduced satellite cell proliferation, and slower rate of protein synthesis. Disruptions in skeletal muscle growth are associated with mitochondrial dysfunction, including reduced pyruvate flux into the mitochondrial matrix and lower complex I activity in the mitochondrial electron transport chain. This review summarizes current research on the mechanisms by which HS-induced placental insufficiency affects skeletal muscle growth in the fetus, with an emphasis on myogenesis, hypertrophy, protein synthesis, and energy metabolism. The evidence presented is primarily drawn from experiments using chronically catheterized fetal sheep exposed to maternal HS during mid-gestation. Additionally, we explore emerging nutritional strategies aimed at enhancing skeletal muscle growth in animals with FGR. These strategies hold promise not only for improving reproductive efficiency in livestock affected by prenatal stress but also for their translational relevance to human pregnancies complicated by placental insufficiency.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e28"},"PeriodicalIF":1.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12478518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}