Journal articles on the topic 'Early life diet'

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1

Sempeski, P., P. Gaudin, H. Persat, and O. Grolet. "Diet selection in early-life stages of grayling (Thymallus thymallus)." Archiv für Hydrobiologie 132, no. 4 (March 10, 1995): 437–52. http://dx.doi.org/10.1127/archiv-hydrobiol/132/1995/437.

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2

Devereux, Graham. "Early life events in asthma—diet." Pediatric Pulmonology 42, no. 8 (2007): 663–73. http://dx.doi.org/10.1002/ppul.20640.

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3

Pérez-Cano, Francisco J., Parveen Yaqoob, Rocío Martín, Margarida Castell Escuer, and Cándido Juárez-Rubio. "Immunonutrition in Early Life: Diet and Immune Development." Clinical and Developmental Immunology 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/207509.

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4

Vaiserman, A. M. "Early-life nutritional programming of longevity." Journal of Developmental Origins of Health and Disease 5, no. 5 (June 13, 2014): 325–38. http://dx.doi.org/10.1017/s2040174414000294.

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Available data from both experimental and epidemiological studies suggest that inadequate diet in early life can permanently change the structure and function of specific organs or homoeostatic pathways, thereby ‘programming’ the individual’s health status and longevity. Sufficient evidence has accumulated showing significant impact of epigenetic regulation mechanisms in nutritional programming phenomenon. The essential role of early-life diet in the development of aging-related chronic diseases is well established and described in many scientific publications. However, the programming effects on lifespan have not been extensively reviewed systematically. The aim of the review is to provide a summary of research findings and theoretical explanations that indicate that longevity can be influenced by early nutrition.
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Lai, Pui Y., Xigang Jing, Teresa Michalkiewicz, Brianna Entringer, Xingrao Ke, Amber Majnik, Alison J. Kriegel, Pengyuan Liu, Robert H. Lane, and Girija G. Konduri. "Adverse early-life environment impairs postnatal lung development in mice." Physiological Genomics 51, no. 9 (September 1, 2019): 462–70. http://dx.doi.org/10.1152/physiolgenomics.00016.2019.

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Background: Fetal growth restriction (FGR) is a major risk factor for bronchopulmonary dysplasia (BPD). Maternal stress and poor diet are linked to FGR. Effect of perinatal stress on lung development remains unknown. Objective: Using a murine model of adverse early life environment (AELE), we hypothesized that maternal exposure to perinatal environmental stress and high-fat diet (Western diet) lead to impaired lung development in the offspring. Methods: Female mice were placed on either control diet or Western diet before conception. Those exposed to Western diet were also exposed to perinatal environmental stress, the combination referred to as AELE. Pups were either euthanized at postnatal day 21 (P21) or weaned to control diet and environment until adulthood (8–14 wk old). Lungs were harvested for histology, gene expression by quantitative RT-PCR, microRNA profiling, and immunoblotting. Results: AELE increased the mean linear intercept and decreased the radial alveolar count and secondary septation in P21 and adult mice. Capillary count was also decreased in P21 and adult mice. AELE lungs had decreased vascular endothelial growth factor A (VEGFA), VEGF receptor 2, endothelial nitric oxide synthase, and hypoxia inducible factor-1α protein levels and increased expression of genes that regulate DNA methylation and upregulation of microRNAs that target genes involved in lung development at P21. Conclusion: AELE leads to impaired lung alveolar and vascular growth, which persists into adult age despite normalizing the diet and environment at P21. AELE also alters the expression of genes involved in lung remodeling.
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6

Aihie Sayer*, A., and C. Cooper. "Early diet and growth: impact on ageing." Proceedings of the Nutrition Society 61, no. 1 (February 2002): 79–85. http://dx.doi.org/10.1079/pns2001138.

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The modification of ageing by nutritional intervention is well recognised. Post-weaning diet restriction is the only widely reproducible method to slow ageing, but the effects of prenatal and preweaning diet restriction have been less well characterised. There is some evidence that diet restriction instituted in utero or shortly after birth may have an opposite effect and be associated with increased ageing, and recent work suggests that it may shorten lifespan. Interest in this area has been rekindled by the growing body of epidemiological evidence showing that a number of age-related diseases are associated with poor growth and inadequate nutrition in early life. The relevance of this association to structural and functional ageing changes in different systems is now being considered. Work on musculo-skeletal ageing has demonstrated that loss of muscle strength and bone mass is greater in individuals who did not grow well in early life, and a range of studies suggests that maternal, developmental and nutritional factors are important. The underlying mechanisms remain speculative, and it remains to be determined whether they are system-specific or universal throughout the body. A new cohort of subjects aged between 60 and 70 years is being established to investigate how genetic factors interact with growth and nutritional influences to programme musculo-skeletal ageing in later life.
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7

N'guessan, Koffi, David Ternant, François Labarthe, and Hervé Watier. "Lability of IgE Levels Early in Life." Journal of Allergy 2011 (June 20, 2011): 1–2. http://dx.doi.org/10.1155/2011/547389.

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We report a case of a very fast and intriguing decrease in IgE concentrations after exclusion from the diet of any CM lysate in an unusual clinical presentation of cow's milk allergy in an infant. Analysis of IgE kinetics after allergen elimination suggests rapid cessation of IgE biosynthesis and a short IgE half-life.
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8

English, Sinead, and Tobias Uller. "Does early-life diet affect longevity? A meta-analysis across experimental studies." Biology Letters 12, no. 9 (September 2016): 20160291. http://dx.doi.org/10.1098/rsbl.2016.0291.

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Life-history theory predicts that nutrition influences lifespan owing to trade-offs between allocating resources to reproduction, growth and repair. Despite occasional reports that early diet has strong effects on lifespan, it is unclear whether this prediction is generally supported by empirical studies. We conducted a meta-analysis across experimental studies manipulating pre- or post-natal diet and measuring longevity. We found no overall effect of early diet on lifespan. We used meta-regression, considering moderator variables based on experimental and life-history traits, to test predictions regarding the strength and direction of effects that could lead to positive or negative effects. Pre-natal diet manipulations reduced lifespan, but there were no effects of later diet, manipulation type, development mode, or sex. The results are consistent with the prediction that early diet restriction disrupts growth and results in increased somatic damage, which incurs lifespan costs. Our findings raise a cautionary note, however, for placing too strong an emphasis on early diet effects on lifespan and highlight limitations of measuring these effects under laboratory conditions.
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9

Pendergrast, Logan A., Eric C. Leszczynski, Joseph R. Visker, Ashley N. Triplett, and David P. Ferguson. "Early life undernutrition reduces maximum treadmill running capacity in adulthood in mice." Applied Physiology, Nutrition, and Metabolism 45, no. 3 (March 2020): 240–50. http://dx.doi.org/10.1139/apnm-2019-0023.

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Undernutrition during early life causes chronic disease with specific impairments to the heart and skeletal muscle. The purpose of this study was to determine the effects of early life undernutrition on adult exercise capacity as a result of cardiac and skeletal muscle function. Pups were undernourished during gestation (GUN) or lactation (PUN) using a cross-fostering nutritive mouse model. At postnatal day 21, all mice were weaned and refed a control diet. At postnatal day 67, mice performed a maximal treadmill test. Echocardiography and Doppler blood flow analysis was performed at postnatal day 72, following which skeletal muscle cross-sectional area (CSA) and fiber type were determined. Maximal running capacity was reduced (diet: P = 0.0002) in GUN and PUN mice. Left ventricular mass (diet: P = 0.03) and posterior wall thickness during systole (diet × sex: P = 0.03) of GUN and PUN mice was reduced, causing PUN mice to have reduced (diet: P = 0.04) stroke volume. Heart rate of GUN mice showed a trend (diet: P = 0.07) towards greater resting values than other groups. PUN mice had greater CSA of soleus fibers. PUN had a reduced (diet: P = 0.03) proportion of type-IIX fibers in the extensor digitorum longus (EDL) and a greater (diet: P = 0.008) percentage of type-IIB fibers in the EDL. In conclusion, gestational and postnatal undernourishment impairs exercise capacity.
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10

Lagiou, Pagona, Hans-Olov Adami, and Dimitrios Trichopoulos. "Early Life Diet and the Risk for Adult Breast Cancer." Nutrition and Cancer 56, no. 2 (November 2006): 158–61. http://dx.doi.org/10.1207/s15327914nc5602_6.

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11

Bekdash, Rola A. "Early Life Nutrition and Mental Health: The Role of DNA Methylation." Nutrients 13, no. 9 (September 4, 2021): 3111. http://dx.doi.org/10.3390/nu13093111.

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Does the quality of our diet during early life impact our long-term mental health? Accumulating evidence suggests that nutrition interacts with our genes and that there is a strong association between the quality of diet and mental health throughout life. Environmental influences such as maternal diet during pregnancy or offspring diet have been shown to cause epigenetic changes during critical periods of development, such as chemical modifications of DNA or histones by methylation for the regulation of gene expression. One-carbon metabolism, which consists of the folate and methionine cycles, is influenced by the diet and generates S-Adenosylmethinoine (SAM), the main methyl donor for methylation reactions such as DNA and histone methylation. This review provides current knowledge on how the levels of one-carbon metabolism associated micronutrients such as choline, betaine, folate, methionine and B vitamins that play a role in brain function can impact our well-being and mental health across the lifespan. Micronutrients that act as methyl donors for SAM formation could affect global or gene methylation, altering gene expression and phenotype. Strategies should then be adopted to better understand how these nutrients work and their impact at different stages of development to provide individualized dietary recommendations for better mental health outcomes.
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12

Tian, Yuan, Bipin Rimal, Wei Gui, Imhoi Koo, Philip B. Smith, Shigetoshi Yokoyama, and Andrew D. Patterson. "Early Life Polychlorinated Biphenyl 126 Exposure Disrupts Gut Microbiota and Metabolic Homeostasis in Mice Fed with High-Fat Diet in Adulthood." Metabolites 12, no. 10 (September 23, 2022): 894. http://dx.doi.org/10.3390/metabo12100894.

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Evidence supports the potential influence of persistent organic pollutants (POPs) on the pathogenesis and progression of obesity and diabetes. Diet-toxicant interactions appear to be important in diet-induced obesity/diabetes; however, the factors influencing this interaction, especially the early life environmental exposure, are unclear. Herein, we investigated the metabolic effects following early life five-day exposure (24 μg/kg body weight per day) to 3,3′,4,4′,5-pentacholorobiphenyl (PCB 126) at four months after exposure in mice fed with control (CTRL) or high-fat diet (HFD). Activation of aryl hydrocarbon receptor (AHR) signaling as well as higher levels of liver nucleotides were observed at 4 months after PCB 126 exposure in mice, independent of diet status. Inflammatory responses including higher levels of serum cytokines and adipose inflammatory gene expression caused by early life PCB 126 were observed only in HFD-fed mice in adulthood. Notably, early life PCB 126 exposure worsened HFD-induced impaired glucose homeostasis characterized by glucose intolerance and elevated gluconeogenesis and tricarboxylic acid (TCA) cycle flux without worsening the effects of HFD related to adiposity in adulthood. Furthermore, early life PCB 126 exposure resulted in diet-dependent changes in bacterial community structure and function later in life, as indicated by metagenomic and metabolomic analyses. These data contribute to a more comprehensive understanding of the interactions between diet and early life environmental chemical exposure.
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13

Murphy, Michelle, and Julian G. Mercer. "Diet-Regulated Anxiety." International Journal of Endocrinology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/701967.

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A substantial proportion of noncommunicable disease originates in habitual overconsumption of calories, which can lead to weight gain and obesity and attendant comorbidities. At the other end of the spectrum, the consequences of undernutrition in early life and at different stages of adult life can also have major impact on wellbeing and quality of life. To help address some of these issues, greater understanding is required of interactions with food and contemporary diets throughout the life course and at a number of different levels: physiological, metabolic, psychological, and emotional. Here we review the current literature on the effects of dietary manipulation on anxiety-like behaviour. This evidence, assembled from study of preclinical models of diet challenge from gestation to adult life, supports a role for diet in the important connections between psychology, physiology, and behaviour. Analogous processes in the human population in our current obesogenic environment are likely to contribute to individual and societal challenges in this area.
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14

Latimore, Janis. "Life without Milk." Nutrition and Food Processing 3, no. 2 (August 17, 2020): 01. http://dx.doi.org/10.31579/2637-8914/026.

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This op-ed article is a metaphor, bemoaning life without the cruelty, brutality, and murder of minorities by police. It indicates the similarities in not needing milk nor police when it is intolerant to survival. Milk is an important nutrient, staple, and a source of calcium for the purpose of supplementing the health in children’s development and for adults in need of additional, calcium-rich foods. Milk is known to build bone development and density. Milk has a long history in the “western diet” (Dalsgaard, Bertram 2015) (standard American diet), as an important nutrient, representative as a valuable source for the human body. In validating food “intake biomarkers (a measurable substance in an organism whose presence is indicative of some phenomenon, such as disease, infection, or environmental exposure), milk becomes part of the human biofluid (a generic term for bio-organic fluid produced by an organism such as, serum, plasma, urine, saliva, and so on” (Dalsgaard, Bertram 2015). We are taught by our parents and advised by natal-conscious doctors, that children cannot grow or maintain a healthy life as babies, pre-k, young adults or grown-ups, if we don’t drink milk or have a diet of milk by-products. But in 1972, early research found; “Negroes” (Paige, Bayless, Graham 1972), Asians, American Indians, Hispanic, South Americans and Black Heritage (American Family Physician, 2006), had trouble digesting an enzyme that breaks down the natural sugar in milk and the same intestinal intolerance arrives in significant numbers when this same group of people within the greater population are in the presence of police.
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15

Toh, Huishi, James A. Thomson, and Peng Jiang. "Maternal High-Fiber Diet Protects Offspring against Type 2 Diabetes." Nutrients 13, no. 1 (December 30, 2020): 94. http://dx.doi.org/10.3390/nu13010094.

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Previous studies have reported that maternal malnutrition is linked to increased risk of developing type 2 diabetes in adulthood. Although several diabetic risk factors associated with early-life environment have been identified, protective factors remain elusive. Here, we conducted a longitudinal study with 671 Nile rats whereby we examined the interplay between early-life environment (maternal diet) and later-life environment (offspring diet) using opposing diets that induce or prevent diet-induced diabetes. Specifically, we modulated the early-life environment throughout oogenesis, pregnancy, and nursing by feeding Nile rat dams a lifelong high-fiber diet to investigate whether the offspring are protected from type 2 diabetes. We found that exposure to a high-fiber maternal diet prior to weaning significantly lowered the risk of diet-induced diabetes in the offspring. Interestingly, offspring consuming a high-fiber diet after weaning did not develop diet-induced diabetes, even when exposed to a diabetogenic maternal diet. Here, we provide the first evidence that the protective effect of a high-fiber diet can be transmitted to the offspring through the maternal diet, which has important implications in diabetes prevention.
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16

Kashtanova, Daria A., Anna S. Popenko, Olga N. Tkacheva, Alexander B. Tyakht, Dimitry G. Alexeev, and Sergey A. Boytsov. "Association between the gut microbiota and diet: Fetal life, early childhood, and further life." Nutrition 32, no. 6 (June 2016): 620–27. http://dx.doi.org/10.1016/j.nut.2015.12.037.

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17

Knutie, Sarah A., Lauren A. Shea, Marinna Kupselaitis, Christina L. Wilkinson, Kevin D. Kohl, and Jason R. Rohr. "Early-Life Diet Affects Host Microbiota and Later-Life Defenses Against Parasites in Frogs." Integrative and Comparative Biology 57, no. 4 (June 28, 2017): 732–42. http://dx.doi.org/10.1093/icb/icx028.

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18

Tang, Ying, Ting-Chun Lin, Soonkyu Chung, Young-Cheul Kim, and Zhenhua Liu. "Impact of High-Fat Diet in Early-Life on Mammary Metabolic and Inflammatory Status in Later-Life in Mice." Current Developments in Nutrition 5, Supplement_2 (June 2021): 54. http://dx.doi.org/10.1093/cdn/nzab033_054.

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Abstract Objectives Emerging evidence indicates a potentially important role for early-life events and exposures in cancer development later in life. Moreover, accumulating evidence suggests that the incidence of cancers has reached a plateau in elders, whereas it continuously rises in young to middle adult. The present study aimed to investigate the potential impacts of high-fat diet in early-life, mimicking childhood/adolescent in humans, on mammary health in later-life of mice, equivalent to the young to middle age in human. Methods Female C57BL/8 mice (4 weeks of age) were fed a low-fat diet (LF: 10% kcal from fat) or a high-fat diet (HF: 60% kcal from fat) for 8 weeks, which is equivalent to child/adolescent age in humans. Mice in early-life groups were sacrificed after 8 weeks feeding, whereas mice in later-life groups were switched to standard chow diet (Lab Diet#5P76) and fed for additional 12 weeks before sacrifice. A panel of metabolic parameters, inflammatory cytokines, as well as gene expression related to tumorigenic Wnt-signaling were assessed by qPCR and immunoblotting analysis. Results Compared with LF group, the body weight in HF group was significantly elevated after 8-wk HF diet feeding (P < 0.05). After switching to the standard chow diet for 12 weeks, the significance remained until 24 weeks of age although with a reduced degree of magnitude (P < 0.05). For the metabolic factors, HFD reduced the expression levels of both Pparγ (P = 0.08) and adiponectin (P < 0.05) at 12 weeks and the reductions remains at 24 weeks (P < 0.01). Meanwhile, expressions of aromatase, estrogen receptor α and Tnf-α, Il-6, Il-10 as well as Cox2 among examined inflammatory mediators (Tnf-α, Il-6, Il-10, Il-2, Il-1β, Ifn-γ, Cox2) were significantly higher in HF than in LF group at 24 weeks (P < 0.05). For Wnt-signaling target genes (Cyclin D1, C-Myc, and Axin 2), a significant increase for C-Myc was observed in HF group at 12 weeks (P < 0.01). Conclusions Our results suggested that HF diet in early-life enhances adiposity and alters mammary metabolic and inflammatory status, creating a microenvironment in favor of breast tumorigenesis in later-life. Funding Sources This project was supported by USDA/Hatch (#1013548).
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19

Beleza, Jorge, Jelena Stevanović-Silva, Pedro Coxito, Hugo Rocha, Paulo Santos, António Ascensão, Joan Ramon Torrella, and José Magalhães. "Gestational Exercise Increases Male Offspring’s Maximal Workload Capacity Early in Life." International Journal of Molecular Sciences 23, no. 7 (April 1, 2022): 3916. http://dx.doi.org/10.3390/ijms23073916.

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Mothers’ antenatal strategies to improve the intrauterine environment can positively decrease pregnancy-derived intercurrences. By challenging the mother–fetus unit, gestational exercise (GE) favorably modulates deleterious stimuli, such as high-fat, high-sucrose (HFHS) diet-induced adverse consequences for offspring. We aimed to analyze whether GE alters maternal HFHS-consumption effects on male offspring’s maximal workload performance (MWP) and in some skeletal muscle (the soleus—SOL and the tibialis anterior—TA) biomarkers associated with mitochondrial biogenesis and oxidative fitness. Infant male Sprague-Dawley rats were divided into experimental groups according to mothers’ dietary and/or exercise conditions: offspring of sedentary control diet-fed or HFHS-fed mothers (C–S or HFHS–S, respectively) and of exercised HFHS-fed mothers (HFHS–E). Although maternal HFHS did not significantly alter MWP, offspring from GE dams exhibited increased MWP. Lower SOL AMPk levels in HFHS–S were reverted by GE. SOL PGC-1α, OXPHOS C-I and C-IV subunits remained unaltered by maternal diet, although increased in HFHS–E offspring. Additionally, GE prevented maternal diet-related SOL miR-378a overexpression, while upregulated miR-34a expression. Decreased TA C-IV subunit expression in HFHS–S was reverted in HFHS–E, concomitantly with the downregulation of miR-338. In conclusion, GE in HFHS-fed dams increases the offspring’s MWP, which seems to be associated with the intrauterine modulation of SM mitochondrial density and functional markers.
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20

Jarocka-Cyrta, E., N. Perin, M. Keelan, E. Wierzbicki, T. Wierzbicki, M. T. Clandinin, and A. B. R. Thomson. "Early dietary experience influences ontogeny of intestine in response to dietary lipid changes in later life." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 2 (August 1, 1998): G250—G258. http://dx.doi.org/10.1152/ajpgi.1998.275.2.g250.

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This study was undertaken to test the hypothesis that a change in the mother’s diet at the time of birth and continued during suckling modifies the intestinal transport of nutrients in the suckling offspring. Pregnant rat dams were fed one of four semisynthetic diets during pregnancy [high or low n-6/n-3 diet or a diet enriched with arachidonic acid (AA) or docosahexaenoic acid (DHA)] and were fed the same diet at the time of birth or switched to another diet. The greatest body weight gain was in the suckling rats (15–16 days of age) fed a low n-6/n-3 diet. Switching from this diet caused weight loss, and the observed weight gain with the low n-6/n-3 diet was prevented by previous exposure of the mother to the high n-6/n-3 diet or the AA- or DHA-containing diet. Although continuous feeding of a high n-6/n-3 diet to the mother during pregnancy and lactation was associated with the lowest in vitro rates of fructose uptake, switching the mother to another diet during lactation did not necessarily correct the low absorption. In contrast, continuous feeding of a high n-6/n-3 diet to the mother during pregnancy and lactation is associated with the highest maximal transport rate of glucose uptake into the jejunum and ileum. Jejunal uptake of fatty acids 12:0, 18:0, 18:3(n-3), and cholesterol was less with the low n-6/n-3 diet compared with the high n-6/n-3 diet, whereas the ileal uptake of 18:0 and 18:3(n-3) was higher with the low n-6/n-3 diet. Thus the ontogeny of the intestine is critically influenced by the mother’s diet during gestation as well as during the nursing period. Some of the diet-associated changes in nutrient uptake resulting from the mother’s diet during pregnancy could be corrected by dietary interventions introduced after birth.
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21

Crisóstomo, Luís, Romeu A. Videira, Ivana Jarak, Kristina Starčević, Tomislav Mašek, Luís Rato, João F. Raposo, Rachel L. Batterham, Pedro F. Oliveira, and Marco G. Alves. "Diet during early life defines testicular lipid content and sperm quality in adulthood." American Journal of Physiology-Endocrinology and Metabolism 319, no. 6 (December 1, 2020): E1061—E1073. http://dx.doi.org/10.1152/ajpendo.00235.2020.

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Childhood obesity is a serious concern associated with ill health later in life. Emerging data suggest that obesity has long-term adverse effects upon male sexual and reproductive health, but few studies have addressed this issue. We hypothesized that exposure to high-fat diet during early life alters testicular lipid content and metabolism, leading to permanent damage to sperm parameters. After weaning ( day 21 after birth), 36 male mice were randomly divided into three groups and fed with a different diet regimen for 200 days: a standard chow diet (CTRL), a high-fat diet (HFD) (carbohydrate: 35.7%, protein: 20.5%, and fat: 36.0%), and a high-fat diet for 60 days, then replaced by standard chow (HFDt). Biometric and metabolic data were monitored. Animals were then euthanized, and tissues were collected. Epididymal sperm parameters and endocrine parameters were evaluated. Testicular metabolites were extracted and characterized by 1H-NMR and GC-MS. Testicular mitochondrial and antioxidant activity were evaluated. Our results show that mice fed with a high-fat diet, even if only until early adulthood, had lower sperm viability and motility, and higher incidence of head and tail defects. Although diet reversion with weight loss during adulthood prevents the progression of metabolic syndrome, testicular content in fatty acids is irreversibly affected. Excessive fat intake promoted an overaccumulation of proinflammatory n-6 polyunsaturated fatty acids in the testis, which is strongly correlated with negative effects upon sperm quality. Therefore, the adoption of high-fat diets during early life correlates with irreversible changes in testicular lipid content and metabolism, which are related to permanent damage to sperm quality later in life.
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Abbink, Maralinde R., Lidewij Schipper, Eva F. G. Naninck, Cato M. H. de Vos, Romy Meier, Eline M. van der Beek, Paul J. Lucassen, and Aniko Korosi. "The Effects of Early Life Stress, Postnatal Diet Modulation, and Long-Term Western-Style Diet on Later-Life Metabolic and Cognitive Outcomes." Nutrients 12, no. 2 (February 22, 2020): 570. http://dx.doi.org/10.3390/nu12020570.

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Early life stress (ES) increases the risk to develop metabolic and brain disorders in adulthood. Breastfeeding (exclusivity and duration) is associated with improved metabolic and neurocognitive health outcomes, and the physical properties of the dietary lipids may contribute to this. Here, we tested whether early life exposure to dietary lipids mimicking some physical characteristics of breastmilk (i.e., large, phospholipid-coated lipid droplets; Concept Nuturis® infant milk formula (N-IMF)), could protect against ES-induced metabolic and brain abnormalities under standard circumstances, and in response to prolonged Western-style diet (WSD) in adulthood. ES was induced by exposing mice to limited nesting material from postnatal day (P) 2 to P9. From P16 to P42, male offspring were fed a standard IMF (S-IMF) or N-IMF, followed by either standard rodent diet (SD) or WSD until P230. We then assessed body composition development, fat mass, metabolic hormones, hippocampus-dependent cognitive function, and neurogenesis (proliferation and survival). Prolonged WSD resulted in an obesogenic phenotype at P230, which was not modulated by previous ES or N-IMF exposure. Nevertheless, ES and N-IMF modulated the effect of WSD on neurogenesis at P230, without affecting cognitive function, highlighting programming effects of the early life environment on the hippocampal response to later life challenges at a structural level.
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Rincel, M., A. L. Lépinay, P. Delage, J. Fioramonti, V. S. Théodorou, S. Layé, and M. Darnaudéry. "Maternal high-fat diet prevents developmental programming by early-life stress." Translational Psychiatry 6, no. 11 (November 2016): e966-e966. http://dx.doi.org/10.1038/tp.2016.235.

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Darnaudéry, Muriel, Marion Rincel, Lépinay Amandine, Delage Pauline, Théodorou Vassilia, and Layé Sophie. "Maternal high-fat diet prevents developmental programming by early life stress." Psychoneuroendocrinology 71 (September 2016): 64. http://dx.doi.org/10.1016/j.psyneuen.2016.07.165.

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Dong, Tien S., and Arpana Gupta. "Influence of Early Life, Diet, and the Environment on the Microbiome." Clinical Gastroenterology and Hepatology 17, no. 2 (January 2019): 231–42. http://dx.doi.org/10.1016/j.cgh.2018.08.067.

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Bokulich, Nicholas A., Jennifer Chung, Thomas Battaglia, Nora Henderson, Melanie Jay, Huilin Li, Arnon D. Lieber, et al. "Antibiotics, birth mode, and diet shape microbiome maturation during early life." Science Translational Medicine 8, no. 343 (June 15, 2016): 343ra82. http://dx.doi.org/10.1126/scitranslmed.aad7121.

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27

Ashwell, Christopher M., and Roselina Angel. "Nutritional genomics: a practical approach by early life conditioning with dietary phosphorus." Revista Brasileira de Zootecnia 39, suppl spe (July 2010): 268–78. http://dx.doi.org/10.1590/s1516-35982010001300030.

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The recent technologies that have led to the new field of functional genomics (how the genome of an organism regulates homeostasis and responds to stimuli) are providing a clearer understanding of how organisms interact with their environment and in particular their diet. We are beginning to learn how the diet may have long-term influence on performance and health. A form of epigenetic regulation has been recently described called fetal "programming". Fueled by epidemiological data the "fetal origins" hypothesis suggests that a poor in utero environment resulting from maternal dietary or placental insufficiency may "program" susceptibility in the fetus to cardiovascular or metabolic disorders. We have observed similar apparent programming by dietary manipulation in the chicken. When birds are challenged with a diet low in phosphorus (P) for 90 hours post-hatch they obtain the ability to better utilize P later in life. This increased retention of P from the diet can partially be explained by an enduring increase in the expression of the intestine-specific Na/P cotransporter (NaPcoT) gene during programming as well as later in life when fed P restricted diets. The resulting data provide the first evidence for neonatal programming of gene expression in an oviparous species.
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Sikalidis, Angelos K., Anita H. Kelleher, and Aleksandra S. Kristo. "Mediterranean Diet." Encyclopedia 1, no. 2 (April 25, 2021): 371–87. http://dx.doi.org/10.3390/encyclopedia1020031.

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The Mediterranean diet is a food pattern incorporated into a set of lifestyle practices typical of Greece and Southern Italy in the early 1960s, where adult life expectancy was notably high, while rates of diet-related chronic diseases were low. The Mediterranean diet was described initially by the work of LG Allbaugh, commissioned by the Rockefeller foundation and the Greek government post-WW2 on the Greek island of Crete in 1948. The Mediterranean diet was accepted as Intangible Cultural Heritage of Humanity by UNESCO in 2013. The primary advantages of the Mediterranean diet include health benefits pertinent to cardiovascular, metabolic syndrome, and cognition.
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Kathrani, Aarti, Emily Jayne Blackwell, Jessica L. Williams, Tim Gruffydd-Jones, Jane K. Murray, Melanie Hezzell, and Edward J. Hall. "Exploring early life events including diet in cats presenting for gastrointestinal signs in later life." Veterinary Record 185, no. 5 (June 5, 2019): 144. http://dx.doi.org/10.1136/vr.105040.

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Our study aimed to determine if certain early life events were more prevalent in cats presenting to veterinary practices specifically for gastrointestinal signs on at least two occasions between six months and 30 months of age. Data from an owner-completed questionnaire for 1212 cats before 16 weeks of age and subsequent questionnaires for the same cats between six months and 30 months of age were reviewed. Of the 1212 cats included, 30 visited a veterinary practice for gastrointestinal signs on two or more occasions. Of the early life events recorded, cats reported with vomiting, diarrhoea or both, and/or those not exclusively fed commercial diet(s) that meets the World Small Animal Veterinary Association (WSAVA) Global Nutrition Committee (GNC) guidelines before 16 weeks of age were more likely to visit veterinary practices specifically for gastrointestinal signs on at least two occasions between six months and 30 months of age (P<0.001, odds ratio (OR)=2.64, 95 per cent confidence interval (CI)=1.66–4.22 and P=0.030, OR=1.51, 95 per cent CI=1.04–2.22, respectively). Ensuring cats exclusively consume commercial diet(s) that meets the WSAVA GNC guidelines and further studies identifying specific aetiologies for vomiting and diarrhoea before 16 weeks of age to enable prevention may reduce the number of cats subsequently presenting to primary care veterinary practices for repeated gastrointestinal signs.
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Joung, Sangyun, Joanne E. Fil, Anne B. Heckmann, Anne S. Kvistgaard, and Ryan N. Dilger. "Early-Life Supplementation of Bovine Milk Osteopontin Supports Neurodevelopment and Influences Exploratory Behavior." Nutrients 12, no. 8 (July 24, 2020): 2206. http://dx.doi.org/10.3390/nu12082206.

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Introduction: Osteopontin (OPN) is a whey protein found at high concentration in human milk and is involved in processes such as bone cell proliferation and differentiation. Milk OPN has shown to be involved in various aspects of development, including the immune system and gut health. However, the influence of dietary bovine milk OPN inclusion on brain and cognitive development has not been studied extensively until recently. This research examines whether dietary supplementation of bovine milk OPN supports brain and cognitive development in the translational pig model. Methods: From postnatal day (PND) 2 to 34, twenty-one intact male pigs were provided ad libitum access to one of two dietary treatments, a standard soy protein isolate-based milk replacer to serve as a control diet (n = 11) and the same base diet supplemented with bovine milk OPN to serve as a test diet (n = 10). In addition to growth and health outcomes, recognition memory was tested using the novel object recognition (NOR) task from PND 28 to 32, and magnetic resonance imaging was conducted at PND 34 to evaluate brain development. Results: No dietary effects were observed for growth performance or health indices. For the behavioral analysis, pigs that received the test diet exhibited shorter (p < 0.05) latency to the first object visited compared with pigs fed the control diet. Although the control group exhibited novelty preference, there was no difference in recognition index between dietary groups. Neuroimaging outcomes revealed increased (p < 0.05) relative brain volumes of the corpus callosum, lateral ventricle, left and right internal capsule, left and right putamen-globus pallidus, and right hippocampus, and right cortex in the test group. Diffusion tensor imaging revealed higher (p < 0.05) radial diffusivity in the corpus callosum and lower (p < 0.05) fractional anisotropy in pigs provided the test diet. Conclusion: Dietary supplementation of bovine milk OPN increased the relative volume of several brain regions and altered behaviors in the NOR task. Underlying mechanisms of bovine milk OPN influencing the development of brain structures and additional behaviors warrant further investigation.
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Pérez-Cano, Francisco J., Àngels Franch, Cristina Castellote, and Margarida Castell. "The Suckling Rat as a Model for Immunonutrition Studies in Early Life." Clinical and Developmental Immunology 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/537310.

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Diet plays a crucial role in maintaining optimal immune function. Research demonstrates the immunomodulatory properties and mechanisms of particular nutrients; however, these aspects are studied less in early life, when diet may exert an important role in the immune development of the neonate. Besides the limited data from epidemiological and human interventional trials in early life, animal models hold the key to increase the current knowledge about this interaction in this particular period. This paper reports the potential of the suckling rat as a model for immunonutrition studies in early life. In particular, it describes the main changes in the systemic and mucosal immune system development during rat suckling and allows some of these elements to be established as target biomarkers for studying the influence of particular nutrients. Different approaches to evaluate these immune effects, including the manipulation of the maternal diet during gestation and/or lactation or feeding the nutrient directly to the pups, are also described in detail. In summary, this paper provides investigators with useful tools for better designing experimental approaches focused on nutrition in early life for programming and immune development by using the suckling rat as a model.
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Mahanes, Timothy M., Margaret O. Murphy, An Ouyang, Frederique B. Yiannikouris, Bradley S. Fleenor, and Analia S. Loria. "Maternal separation-induced increases in vascular stiffness are independent of circulating angiotensinogen levels." Journal of Applied Physiology 129, no. 1 (July 1, 2020): 58–65. http://dx.doi.org/10.1152/japplphysiol.00703.2019.

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This study demonstrates that there was no correlation between circulating levels of angiotensinogen (AGT) and the development of vascular stiffness in rats exposed to early-life stress and fed a normal diet. This study also shows that early-life stress-induced hypersensitive vascular contractility to angiotensin II in rats fed a high-fat diet is independent of circulating levels of AGT and occurs without further progression of vascular stiffness. Our data show that early-life stress primes the adipose tissue to secrete AGT in a sex- and species-independent fashion.
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Noguera, José C., Marta Lores, Carlos Alonso-Álvarez, and Alberto Velando. "Thrifty development: early-life diet restriction reduces oxidative damage during later growth." Functional Ecology 25, no. 5 (April 28, 2011): 1144–53. http://dx.doi.org/10.1111/j.1365-2435.2011.01856.x.

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34

Thiel, R., T. Mehner, B. Kopcke, and R. Kafemann. "Diet Niche Relationships among Early Life Stages of Fish in German Estuaries." Marine and Freshwater Research 47, no. 2 (1996): 123. http://dx.doi.org/10.1071/mf9960123.

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Diet composition, selectivity, food niche width and food niche overlap of early life stages of fishes were studied in the Barther Bodden system and in the Weser and Elbe estuaries during spring and summer from 1987 to 1991 and from 1993 to 1994. Larvae of perch (Perca fluviatilis) and roach (Rutilus rutilus) dominated in the Barther Bodden. Herring (Clupea harengus) and perch were the dominant species in the Barther Strom. Smelt (Osmerus eperlanus) was the most common species in the Elbe estuary. Sprat (Sprattus sprattus) was of most importance in the Weser estuary. The dominant prey of fish larvae were copepodids, nauplii and eggs of Eurytemora afinis. The highest food niche width was observed for nine-spined stickleback (Pungitius pungitius), ruffe (Gymnocephalus cernuus), three-spined stickleback (Gasterosteus aculeatus) and perch in the Barther Bodden. Negative selectivity indices indicated that populations of rotifers were scarcely influenced by predation by fish larvae. In contrast, E. affinis was preferred by early life stages of fish. Positive relationships were estimated between maximum prey lengths and predator lengths of different fish species. Key species with regard to niche overlap were nine-spined stickleback, roach, three-spined stickleback and perch in the Barther Bodden, perch and herring in the Barther Strom, herring and three-spined stickleback in the Elbe estuary, and sprat and common goby (Pomatoschisrus microps) in the Weser estuary. High geographical overlap between fish species occurred in the Elbe estuary and Barther Bodden, whereas high diet overlap was estimated for both the Weser estuary and Barther Strom.
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Morris, Margaret J., Vivian Le, and Jayanthi Maniam. "The impact of poor diet and early life stress on memory status." Current Opinion in Behavioral Sciences 9 (June 2016): 144–51. http://dx.doi.org/10.1016/j.cobeha.2016.04.002.

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36

Segar, Jeffrey L., Connie C. Grobe, Kirthikaa Balapattabi, McKenzie L. Ritter, John J. Reho, and Justin L. Grobe. "Dissociable effects of dietary sodium in early life upon somatic growth, fluid homeostasis, and spatial memory in mice of both sexes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 4 (April 1, 2021): R438—R451. http://dx.doi.org/10.1152/ajpregu.00281.2020.

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Postnatal growth failure is a common morbidity for preterm infants and is associated with adverse neurodevelopmental outcomes. Although sodium (Na) deficiency early in life impairs somatic growth, its impact on neurocognitive functions has not been extensively studied. We hypothesized that Na deficiency during early life is sufficient to cause growth failure and program neurobehavioral impairments in later life. C57BL/6J mice were placed on low- (0.4), normal- (1.5), or high- (3 g/kg) Na chow at weaning ( PD22) and continued on the diet for 3 wk (to PD40). Body composition and fluid distribution were determined serially by time-domain NMR and bioimpedance spectroscopy, and anxiety, learning, and memory were assessed using the elevated plus maze and Morris water maze paradigms in later adulthood ( PD63– PD69). During the diet intervention, body mass gains were suppressed in the low- compared with normal- and high-Na groups despite similar caloric uptake rates across groups. Fat mass was reduced in males but not in females fed low-Na diet. Fat-free mass and hydration were significantly reduced in both males and females fed the low-Na diet, although rapidly corrected after return to normal diet. Measures of anxiety-like behavior and learning in adulthood were not affected by diet in either sex, yet memory performance was modified by a complex interaction between sex and early life Na intake. These data support the concepts that Na deficiency impairs growth and that the amount of Na intake which supports optimal somatic growth during early life may be insufficient to fully support neurocognitive development.
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37

Lee, Seunghyung, Shaowei Zhai, Dong-Fang Deng, Yuquan Li, Patrick Christopher Blaufuss, Bradley T. Eggold, and Fred Binkowski. "Feeding Strategies for Adapting Lake Sturgeon (Acipenser fulvescens) Larvae to Formulated Diets at Early Life Stages." Animals 12, no. 22 (November 13, 2022): 3128. http://dx.doi.org/10.3390/ani12223128.

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Cost-effective feeding management is required to support conservation hatcheries for lake sturgeon (Acipenser fulvescens), an ecologically important species in the Great Lakes region. This study investigated an approach to transition lake sturgeon larvae from live feed (Artemia) to formulated feed and its effect on growth performance, survival, and response to acute hypoxia stress. The first experiment showed that sturgeon had similar (p > 0.05) growth and survival when fed Artemia or the combined feeding of Artemia with the commercial diet (crude protein, 551 g/kg diet). Feeding solely on the commercial or lab-made (crude protein, 491 g/kg diet) diet significantly reduced growth and survival (p < 0.05). In the second experiment, the growth performance of sturgeon (14 days post-hatch, DPH) fed with either Artemia only or combined feeding different feeding durations of two, three, and four weeks followed by a complete transition to the commercial diet. At the end of six weeks, the 3- and 4-week combined feeding periods resulted in significantly higher body weight and survival compared to the 2-week combined and the Artemia only feeding treatments. In the last experiment, sturgeons (27 DPH) were fed only with Artemia or combined feeding of Artemia with the commercial diet for four weeks followed by the complete transition to the commercial diet for two weeks. Eighteen fish from each treatment were investigated the response to acute hypoxic conditions (gradual decrease in dissolved oxygen level from 8 to 2.3 mg/L at the rate of 1 mg/L per hour). When the dissolved oxygen was between 3 and 4 mg/L, the mortality rate of the combination-fed sturgeon (11.7%) was significantly lower than those fed only Artemia (83.3%). These results clearly demonstrate that a commercial diet can partially replace Artemia at early life stages to improve growth, survival, and hypoxia tolerance and thus its co-feeding with Artemia is recommended.
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38

Chandra, Ranjit Kumar. "Food allergy and nutrition in early life: implications for later health." Proceedings of the Nutrition Society 59, no. 2 (May 2000): 273–77. http://dx.doi.org/10.1017/s0029665100000306.

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Allergic diseases are a common cause of illness in most industrialized countries. Diet during early childhood is an important determinant of the development of allergy, particularly in high-risk infants who have a parental history of atopy. Maternal avoidance of highly-allergenic foods during pregnancy and lactation, prolonged exclusive breast-feeding, the use of a hydrolysed milk formula, and delayed introduction of dairy products, eggs, fish, nuts and soyabean are associated with a lower incidence of allergic symptoms and signs. These beneficial effects are observed for as long as 18 years of age. Similarly, nutrition and physical growth are important factors that influence immunocompetence and morbidity due to infections. Small-for-gestational age low-birth-weight infants show prolonged impairment of cell-mediated immunity, antibody responses and phagocyte function. Recent studies indicate the beneficial effect of moderate amounts of Zn given in the first 6 months of life. Thus, diet and nutrition in early life are crucial for the development of allergic and infectious disease throughout childhood and into adulthood.
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Waisbren, Susan E., Barbara E. Mahon, Richard R. Schnell, and Harvey L. Levy. "Predictors of Intelligence Quotient and Intelligence Quotient Change in Persons Treated for Phenylketonuria Early in Life." Pediatrics 79, no. 3 (March 1, 1987): 351–55. http://dx.doi.org/10.1542/peds.79.3.351.

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Ninety-one individuals with phenylketonuria who were treated early in life were followed for as many as 22 years. Regression analyses were used to determine the best predictors of IQ and IQ change. Among treatment-related variables, good dietary control of the blood phenylalanine level stood out as the best predictor of IQ. Diet discontinuation and the natural (off diet) blood phenylalanine level best predicted IQ loss, suggesting that diet continuation may be important for children with natural blood phenylalanine levels greater than 18 mg/dL.
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40

Godbout, J., M. Wulczynski, H. J. Galipeau, M. Constante, T. Ribeiro, D. Sloboda, and E. Verdu. "A10 EARLY LIFE SENSITIZATION TO GLUTEN INDUCES SUSTAINED IMMUNOPATHOLOGY IN DR3-DQ2 MICE." Journal of the Canadian Association of Gastroenterology 5, Supplement_1 (February 21, 2022): 11–13. http://dx.doi.org/10.1093/jcag/gwab049.009.

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Abstract Background Celiac disease (CeD) is an autoimmune T-cell mediated enteropathy, triggered by gluten, a group of proteins found in wheat, barley, and rye. The defined role of gluten as a dietary trigger, necessary genes (HLA-DQ2 and/or DQ8), and tissue transglutaminase (TG2) as the autoantigen together, are unique features of CeD. Although CeD onset can occur at any age, first dietary introduction of gluten during infancy is a critical window of exposure, especially in infants homozygous for the HLA DQ2.5 allele. While adult sensitization studies have been recently performed in DR3-DQ2 mice, the consequences of early life gluten sensitization timing remain unexplored. Aims Our aim was to characterize gluten-immunopathology and CeD-specific serology in specific pathogen free (SPF) DR3-DQ2 transgenic mice sensitized to gluten, 1 week before weaning. Methods Seven-week-old SPF DR3-DQ2 transgenic mice, kept on a gluten-free diet (GFD), were paired for breeding. At post-natal day 3, pups were standardized to 4 per litter (n=2 male, n=2 female) to ensure equal nutrition across litters. At 14 days of age, pups were sensitized with pepsin-trypsin digested gliadin and cholera toxin (CT) three times in one week (n=15). At 21 days of age, pups were weaned and placed either on a gluten-containing diet (n=7), (equivalent of 20g/d of gluten in a human diet -high dose-) or an isocaloric GFD (n=8) until 10 weeks of age. Non-sensitized controls (n=7) received only CT and were kept on the GFD. At sacrifice, serum was collected for anti-TG2 and anti-gliadin antibodies (AGA). Jejunal tissue was collected for histological analysis using villus-to-crypt (V/C) ratios and CD3+ intraepithelial lymphocytes (IEL) counts. Results Gluten-sensitized mice placed on a gluten-containing diet post-weaning had lower V/C ratios and higher CD3+ IEL counts compared with controls (p&lt;0.01). Pre-weaning sensitized mice that were kept on a GFD post-weaning had sustained decreases in V/C ratios and higher CD3+ IEL counts (p&lt;0.01). Out of 15 sensitized mice, 7 developed positive anti-gliadin IgA (p=0.02) and 4 had positive anti-TG2 IgA antibodies (p=0.01) in intestinal contents, irrespective of gluten in the diet. None of the controls had detectable AGA or anti-TG2 antibodies. Conclusions Pre-weaning gluten sensitization of DR3-DQ2 mice induced prolonged gluten immunopathology that did not reverse after 5 weeks on a GFD. Our results indicate that young DR3-DQ2 mice are susceptible to gluten sensitization, with sustained immunopathology, suggesting a critical window of vulnerability in familial carriers of DQ2.5. This novel model will be useful to investigate environmental cofactors at the first time of gluten introduction to the diet. Funding Agencies CIHR
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Moody, Laura, Justin Shao, Hong Chen, and Yuan-Xiang Pan. "Maternal Low-Fat Diet Programs the Hepatic Epigenome despite Exposure to an Obesogenic Postnatal Diet." Nutrients 11, no. 9 (September 3, 2019): 2075. http://dx.doi.org/10.3390/nu11092075.

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Obesity and metabolic disease present a danger to long-term health outcomes. It has been hypothesized that epigenetic marks established during early life might program individuals and have either beneficial or harmful consequences later in life. In the present study, we examined whether maternal diet alters DNA methylation and whether such modifications persist after an obesogenic postnatal dietary challenge. During gestation and lactation, male Sprague-Dawley rats were exposed to either a high-fat diet (HF; n = 10) or low-fat diet (LF; n = 10). After weaning, all animals were fed a HF diet for an additional nine weeks. There were no differences observed in food intake or body weight between groups. Hepatic DNA methylation was quantified using both methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme sequencing (MRE-seq). Overall, 1419 differentially methylated regions (DMRs) were identified. DMRs tended to be located in CpG shores and were enriched for genes involved in metabolism and cancer. Gene expression was measured for 31 genes in these pathways. Map3k5 and Igf1r were confirmed to be differentially expressed. Finally, we attempted to quantify the functional relevance of intergenic DMRs. Using chromatin contact data, we saw that conserved DMRs were topologically associated with metabolism genes, which were associated with differential expression of Adh5, Enox1, and Pik3c3. We show that although maternal dietary fat is unable to reverse offspring weight gain in response to a postnatal obesogenic diet, early life diet does program the hepatic methylome. Epigenetic alterations occur primarily in metabolic and cancer pathways and are associated with altered gene expression, but it is unclear whether they bear consequence later in life.
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NGUYEN, THI HANH, and PETER SCHAUSBERGER. "Diet experiences early in life mold individual foraging niches and personalities of omnivorous predatory mites." Zoosymposia 22 (November 30, 2022): 115. http://dx.doi.org/10.11646/zoosymposia.22.1.70.

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The theory of individual niche specialization posits that members of local groups should diversify in their realized individual diet niches to alleviate inter-individual food competition and ensuing conflicts (Bolnick et al. 2003). Here we tested the hypothesis that early life experiences co-shape individual specialization in diet niches and animal personality expression in the omnivorous plant-inhabiting predatory mite Amblyseius swirskii.
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43

Thomson, A. B. R., and M. Keelan. "Rechallenge Following an Early Life Exposure to a High-Cholesterol Diet Enhances Diet-Associated Alterations in Intestinal Permeability." Journal of Pediatric Gastroenterology and Nutrition 9, no. 1 (July 1989): 98–104. http://dx.doi.org/10.1097/00005176-198907000-00018.

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44

Thomson, A. B. R., and M. Keelan. "Rechallenge Following an Early Life Exposure to a High-Cholesterol Diet Enhances Diet-Associated Alterations in Intestinal Permeability." Journal of Pediatric Gastroenterology and Nutrition 9, no. 1 (July 1989): 98–104. http://dx.doi.org/10.1097/00005176-198909010-00018.

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45

Palace, Vince P., and Julieta Werner. "Vitamins A and E in the maternal diet influence egg quality and early life stage development in fish: a review." Scientia Marina 70, S2 (October 30, 2006): 41–57. http://dx.doi.org/10.3989/scimar.2006.70s241.

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46

Senior, A. M., S. Nakagawa, D. Raubenheimer, S. J. Simpson, and D. W. A. Noble. "Dietary restriction increases variability in longevity." Biology Letters 13, no. 3 (March 2017): 20170057. http://dx.doi.org/10.1098/rsbl.2017.0057.

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Nutritional environments, particularly those experienced during early life, are hypothesized to affect longevity. A recent cross-taxa meta-analysis found that, depending upon circumstance, average longevity may be increased or decreased by early-life dietary restriction. Unstudied are the effects of diet during development on among-individual variance in longevity. Here, we address this issue using emerging methods for meta-analysis of variance. We found that, in general, standard deviation (s.d.) in longevity is around 8% higher under early-life dietary restriction than a standard diet. The effects became especially profound when dietary insults were experienced prenatally (s.d. increased by 29%) and/or extended into adulthood (s.d. increased by 36.6%). Early-life dietary restriction may generate variance in longevity as a result of increased variance in resource acquisition or allocation, but the mechanisms underlying these largely overlooked patterns clearly warrant elucidation.
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47

Morley, Ruth. "The influence of early diet on later development." Journal of Biosocial Science 28, no. 4 (October 1996): 481–87. http://dx.doi.org/10.1017/s0021932000022549.

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SummaryThe possibility that early nutrition has long term consequences in man has been much debated. There have been limited opportunities to perform formal randomised studies on the effect of early nutrition in man and many studies have been flawed by problems with study design. Infants born preterm are a special group. At the start of this study in 1982 evidence on which to base choice of diet was inconsistent and related only to short term outcome, and diets available for such babies differed greatly in nutrient content. In this group it was both ethical and practical to conduct a formal, randomised trial of early diet and outcome and the results were clearly needed for management decisions.A long term prospective outcome study was undertaken on 926 preterm infants randomly assigned to the diet received in the neonatal period. Surviving children have been followed at 9 months, 18 months and now 7½–8 years of age. The findings suggest that children fed a nutrient supplemented preterm formula perform better than those fed a standard formula milk, and also that human milk may contain factors which promote brain growth or development. Outcome data from the randomised trials show that a very brief period of dietary manipulation (on average for the first 4 weeks of life) influences later development.
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Mischke, Mona, Tulika Arora, Sebastian Tims, Eefje Engels, Nina Sommer, Kees van Limpt, Annemarie Baars, et al. "Specific synbiotics in early life protect against diet-induced obesity in adult mice." Diabetes, Obesity and Metabolism 20, no. 6 (March 5, 2018): 1408–18. http://dx.doi.org/10.1111/dom.13240.

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49

Parsons, Tessa J., Marijke van Dusseldorp, Martine van Der Vliet, Karen van de Werken, Gertjan Schaafsma, and Wija A. van Staveren. "Reduced Bone Mass in Dutch Adolescents Fed a Macrobiotic Diet in Early Life." Journal of Bone and Mineral Research 12, no. 9 (September 1, 1997): 1486–94. http://dx.doi.org/10.1359/jbmr.1997.12.9.1486.

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50

Darnaudery, Muriel. "Early life stress and high fat diet: From comfort food to nutritional stress." Nutrition Clinique et Métabolisme 34, no. 1 (April 2020): 5. http://dx.doi.org/10.1016/j.nupar.2020.02.005.

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