Academic literature on the topic 'Offspring adiposity'
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Journal articles on the topic "Offspring adiposity"
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Zhang, Jie, Gemma L. Clayton, Stefan Nygaard Hansen, Anja Olsen, Deborah A. Lawlor, and Christina C. Dahm. "Maternal Pre-Pregnancy BMI, Offspring Adiposity in Late Childhood, and Age of Weaning: A Causal Mediation Analysis." Nutrients 15, no. 13 (2023): 2970. http://dx.doi.org/10.3390/nu15132970.
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Infant feeding practices have been hypothesized to influence offspring's body mass index (BMI) later in life, and women with overweight or obesity tend to wean their infants earlier than women with healthy BMI. We, therefore, aimed to investigate how much early age of weaning mediated the maternal-offspring adiposity relationship. The study included 4920 mother-child pairs from the Avon Longitudinal Study of Parents and Children birth cohort. G-computation was applied to estimate the natural direct (NDE) and indirect (NIE) effects, via the age of weaning (<3 months, 3 months, >3 months), of maternal pre-pregnancy overweight or obesity on offspring’s BMI and fat mass index. The NDE of maternal overweight or obesity on offspring BMI at 17 years old was 2.63 kg/m2 (95% CI: 2.27 to 2.99). The NIE via the age of weaning was 0.02 kg/m2 (95% CI: 0.00 to 0.04), corresponding to 0.8% of the total effect. Similar results were observed for the offspring’s fat mass index. The NDE and NIE were similar to the main analyses when we looked at the relationship stratified by breastfeeding status. Our study found a minimal influence of age of weaning on the pathway between maternal and offspring adiposity, indicating the age of weaning may not be a key mediator.
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Krasnow, Stephanie M., My Linh T. Nguyen, and Daniel L. Marks. "Increased maternal fat consumption during pregnancy alters body composition in neonatal mice." American Journal of Physiology-Endocrinology and Metabolism 301, no. 6 (2011): E1243—E1253. http://dx.doi.org/10.1152/ajpendo.00261.2011.
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Maternal overnutrition prior to and during gestation causes pronounced metabolic dysfunction in the adult offspring. However, less is known about metabolic adaptations in the offspring that occur independently of postnatal growth and nutrition. Therefore, we evaluated the impact of excess maternal dietary lipid intake on the in utero programming of body composition, hepatic function, and hypothalamic development in newborn (P0) offspring. Female mice were fed a low-fat (LF) or high-fat (HF) diet and were mated after 4, 12, and 23 wk. A subset of the obese HF dams was switched to the LF diet during the second (DR2) or third (DR3) pregnancies. The HF offspring accrued more fat mass than the LF pups, regardless of duration of maternal HF diet consumption or prepregnancy maternal adiposity. Increased neonatal adiposity was not observed in the DR3 pups. Liver weights were reduced in the HF offspring but not in the DR2 or DR3 pups. Offspring hepatic triglyceride content was reduced in the HF pups, but hepatic inflammation and expression of lipid metabolism genes were largely unaffected by maternal diet. Maternal diet did not alter the hypothalamic expression of orexigenic and anorexigenic neuropeptides in the offspring. Thus, the intrauterine programming of increased neonatal adiposity and reduced liver size by maternal overnutrition is evident in mice at birth and occurs prior to the development of maternal obesity. These observations demonstrate that dietary intervention during pregnancy minimizes the deleterious effects of maternal obesity on offspring body composition, potentially reducing the offsprings' risk of developing obesity and related diseases later in life.
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Mort, Emily J., Sophie Heritage, Susan Jones, Abigail L. Fowden, and Emily J. Camm. "Sex-Specific Effects of a Maternal Obesogenic Diet High in Fat and Sugar on Offspring Adiposity, Growth, and Behavior." Nutrients 15, no. 21 (2023): 4594. http://dx.doi.org/10.3390/nu15214594.
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With rising rates of human obesity, this study aimed to determine the relationship between maternal diet-induced obesity, offspring morphometrics, and behavior in mice. Pregnant and lactating female mice fed a diet high in fat and sugar (HFHS) commonly consumed by human populations showed decreased food, calorie, and protein intake but increased adiposity at the expense of lean mass. The pre-weaning body weight of the HFHS offspring was reduced for the first postnatal week but not thereafter, with HFHS female offspring having higher body weights by weaning due to continuing higher fractional growth rates. Post-weaning, there were minor differences in offspring food and protein intake. Maternal diet, however, affected fractional growth rate and total body fat content of male but not female HFHS offspring. The maternal diet did not affect the offspring’s locomotor activity or social behavior in either sex. Both the male and female HFHS offspring displayed reduced anxiety-related behaviors, with sex differences in particular aspects of the elevated plus maze task. In the novel object recognition task, performance was impaired in the male but not female HFHS offspring. Collectively, the findings demonstrate that maternal obesity alters the growth, adiposity, and behavior of male and female offspring, with sex-specific differences.
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Howie, G. J., D. M. Sloboda, and M. H. Vickers. "Maternal undernutrition during critical windows of development results in differential and sex-specific effects on postnatal adiposity and related metabolic profiles in adult rat offspring." British Journal of Nutrition 108, no. 2 (2011): 298–307. http://dx.doi.org/10.1017/s000711451100554x.
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It is well established that altered maternal nutrition may induce long-term metabolic consequences in offspring. However, the effects of maternal undernutrition during different developmental windows on sex-specific growth and metabolism in offspring are not well defined. We investigated the effect of moderate maternal undernutrition during pregnancy and/or lactation on postnatal growth and metabolic outcomes in offspring. Wistar rats were randomly assigned to one of four groups: (1) control (CONT) dams fed a standard diet throughout pregnancy and lactation; (2) dams undernourished to 50 % of CONT during pregnancy (UNP); (3) dams fed at 50 % of CONT throughout lactation (UNL); (4) dams fed at 50 % of CONT throughout pregnancy and lactation (UNPL). UNP and UNPL offspring were lighter at birth compared to CONT and UNL. UNL and UNPL offspring were growth restricted at weaning and remained smaller into adulthood. UNP males and females developed increased adiposity and hyperleptinaemia in adulthood compared to all other groups. Adiposity in UNL and UNPL males was similar to CONT offspring. In UNL and UNPL females, adiposity was lower than for CONT females. Markers of bone mass, lipid metabolism and hepatic function were altered in UNP offspring but were similar in UNL and UNPL offspring compared to CONT. Lack of catch-up growth during lactation in offspring of undernourished mothers prevented development of adiposity and related metabolic disorders in later life. These data highlight that the timing and duration of undernutrition during critical windows of development exert differential effects on postnatal outcomes in a sex-specific manner.
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Tsai, Ti-An, Chang-Ku Tsai, Li-Tung Huang, et al. "Maternal Resveratrol Treatment Re-Programs and Maternal High-Fat Diet-Induced Retroperitoneal Adiposity in Male Offspring." International Journal of Environmental Research and Public Health 17, no. 8 (2020): 2780. http://dx.doi.org/10.3390/ijerph17082780.
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Obesity during pregnancy increases the risk of cardiovascular problems, diabetes, asthma, and cognitive impairments, affecting the offspring. It is important to reduce the negative effects of obesity and high-fat (HF) diet during pregnancy. We employed a rat model of maternal HF diet to evaluate the possible de-programming effects of resveratrol in rodent male offspring with maternal HF diet/obesity. Male rat offspring were randomized into four groups: maternal control diet/postnatal control diet, maternal HF diet/postnatal control diet, maternal control diet plus maternal resveratrol treatment/postnatal control diet, and maternal HF diet plus maternal resveratrol treatment/postnatal control diet. Maternal HF diet during pregnancy plus lactation resulted in retroperitoneal adiposity in the male offspring. Maternal resveratrol treatment re-programmed maternal HF exposure-induced visceral adiposity. Offspring that received prenatal HF diet showed higher leptin/soluble leptin receptor (sOB-R) ratio than offspring that received prenatal control diet. Maternal resveratrol treatment ameliorated maternal HF exposure-induced increase in leptin/sOB-R ratio and altered the expression of genes for crucial fatty acid synthesis enzymes in the offspring. Thus, maternal resveratrol administration reduces retroperitoneal adiposity in rat offspring exposed to prenatal HF diet/obesity and could be used to ameliorate negative effects of maternal HF diet in the offspring.
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Cervantes-Rodríguez, M., M. Martínez-Gómez, E. Cuevas, et al. "Sugared water consumption by adult offspring of mothers fed a protein-restricted diet during pregnancy results in increased offspring adiposity: the second hit effect." British Journal of Nutrition 111, no. 4 (2013): 616–24. http://dx.doi.org/10.1017/s0007114513003000.
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Poor maternal nutrition predisposes offspring to metabolic disease. This predisposition is modified by various postnatal factors. We hypothesised that coupled to the initial effects of developmental programming due to a maternal low-protein diet, a second hit resulting from increased offspring postnatal sugar consumption would lead to additional changes in metabolism and adipose tissue function. The objective of the present study was to determine the effects of sugared water consumption (5 % sucrose in the drinking-water) on adult offspring adiposity as a ‘second hit’ following exposure to maternal protein restriction during pregnancy. We studied four offspring groups: (1) offspring of mothers fed the control diet (C); (2) offspring of mothers fed the restricted protein diet (R); (3) offspring of control mothers that drank sugared water (C-S); (4) offspring of restricted mothers that drank sugared water (R-S). Maternal diet in pregnancy was considered the first factor and sugared water consumption as the second factor – the second hit. Body weight and total energy consumption, before and after sugared water consumption, were similar in all the groups. Sugared water consumption increased TAG, insulin and cholesterol concentrations in both the sexes of the C-S and R-S offspring. Sugared water consumption increased leptin concentrations in the R-S females and males but not in the R offspring. There was also an interaction between sugared water and maternal diet in males. Sugared water consumption increased adipocyte size and adiposity index in both females and males, but the interaction with maternal diet was observed only in females. Adiposity index and plasma leptin concentrations were positively correlated in both the sexes. The present study shows that a second hit during adulthood can amplify the effects of higher adiposity arising due to poor maternal pregnancy diet in an offspring sex dependent fashion.
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Hammoud, Rola, Emanuela Pannia, Ruslan Kubant, Rebecca Simonian, and G. Harvey Anderson. "High Choline During Pregnancy Reduces Characteristics of the Metabolic Syndrome in Male Wistar Rat Offspring Fed a High Fat Post-Weaning Diet." Current Developments in Nutrition 5, Supplement_2 (2021): 1313. http://dx.doi.org/10.1093/cdn/nzab059_014.
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Abstract Objectives The prenatal period is a critical time for fetal development, programming the offspring's later-life health in response to the postnatal environment. We have shown that a high maternal choline diet programs long-term energy regulation leading to higher food intake and weight-gain in mature rat offspring fed a normal fat diet. However, the offspring's response to an obesogenic post-weaning diet has not been described. We aim to elucidate the interaction between the choline content of the gestational diet (GD) and fat content of the post-weaning diet (PWD) on male Wistar rat offspring's long-term metabolic phenotype. Methods Pregnant Wistar rats were fed an AIN-93G diet with either recommended choline (RC, 1g/kg diet choline bitartrate) or high choline (HC, 2.5-fold). Male pups were weaned to either a normal (10%) fat (RC-NF and HC-NF) or a high (45%) fat (RC-HF and HC-HF) diet for 17 weeks. Dependent measures were body weight, food intake, visceral adiposity, plasma glucoregulatory hormones and triglycerides, and plasma and hepatic free fatty acids (FFAs). Data were analyzed with 2-way ANOVA for main effects of GD and PWD and their interaction. Measures with significant interaction effects were followed by a Student's T-test comparing groups stratified by PWD. Results HC-HF offspring had lower body weight (7%, P &lt; 0.05), and visceral adiposity (15%, P &lt; 0.05), but no difference in food intake compared to RC-HF. HC-HF offspring had lower insulin (18%, P &lt; 0.05), HOMA-IR (24%, P &lt; 0.01), and plasma triglycerides (30%, P &lt; 0.05) but no difference in leptin. Total hepatic ω-3 FFAs (30%, P &lt; 0.05) were higher and ω-6/ω-3 (P &lt; 0.01) was lower in HC-HF compared to RC-HF, indicating an ameliorated metabolic phenotype in HC-HF offspring. In contrast, HC-NF offspring had higher food intake (8%, P &lt; 0.01) and body weight (6%, P &lt; 0.05) and no difference in adiposity compared to RC-NF. They also had higher plasma leptin adjusted for adiposity (22%, P &lt; 0.05) but not insulin or HOMA-IR compared to RC-NF. Hepatic C16:1n-7/C16:0 ratio was higher in HC-NF compared to RC-NF, suggestive of dysregulated lipid metabolism. Conclusions Gestational choline supplementation is associated with improved long-term metabolic regulation in male Wistar rat offspring fed a high fat post-weaning diet. Funding Sources CIHR-Institute of Nutrition, Metabolism, and Diabetes.
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Bianco, Monica E., My H. Vu, James R. Bain, et al. "Maternal and Cord Blood Serum Metabolite Associations with Childhood Adiposity and Body Composition Outcomes." Metabolites 13, no. 6 (2023): 749. http://dx.doi.org/10.3390/metabo13060749.
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Maternal metabolites influence the size of newborns independently of maternal body mass index (BMI) and glycemia, highlighting the importance of maternal metabolism on offspring outcomes. This study examined associations of maternal metabolites during pregnancy with childhood adiposity, and cord blood metabolites with childhood adiposity using phenotype and metabolomic data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study and the HAPO Follow-Up Study. The maternal metabolites analyses included 2324 mother–offspring pairs, while the cord blood metabolites analyses included 937 offspring. Multiple logistic and linear regression were used to examine associations between primary predictors, maternal or cord blood metabolites, and childhood adiposity outcomes. Multiple maternal fasting and 1 hr metabolites were significantly associated with childhood adiposity outcomes in Model 1 but were no longer significant after adjusting for maternal BMI and/or maternal glycemia. In the fully adjusted model, fasting lactose levels were negatively associated with child BMI z-scores and waist circumference, while fasting urea levels were positively associated with waist circumference. One-hour methionine was positively associated with fat-free mass. There were no significant associations between cord blood metabolites and childhood adiposity outcomes. Few metabolites were associated with childhood adiposity outcomes after adjusting for maternal BMI and glucose, suggesting that maternal BMI accounts for the association between maternal metabolites and childhood adiposity.
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Zinkhan, E. K., B. Yu, C. W. Callaway, and R. A. McKnight. "Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring." Journal of Developmental Origins of Health and Disease 9, no. 3 (2018): 315–28. http://dx.doi.org/10.1017/s2040174418000016.
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AbstractIntrauterine growth restriction (IUGR) and fetal exposure to a maternal high-fat diet (HFD) independently increase the risk of developing obesity in adulthood. Excess glucocorticoids increase obesity. We hypothesized that surgically induced IUGR combined with an HFD would increase adiposity and glucocorticoids more than in non-IUGR offspring combined with the same HFD, findings that would persist despite weaning to a regular diet. Non-IUGR (N) and IUGR (I) rat offspring from dams fed either regular rat chow (R) or an HFD (H) were weaned to either a regular rat chow or an HFD. For non-IUGR and IUGR rats, this study design resulted in three diet groups: offspring from dams fed a regular diet and weaned to a regular diet (NRR and IRR), offspring rats from dams fed an HFD and weaned to a regular diet (NHR and IHR) and offspring from dams fed an HFD and weaned to an HFD (NHH and IHH). Magnetic resonance imaging or fasting visceral and subcutaneous adipose tissue collection occurred at postnatal day 60. IHH male rats had greater adiposity than NHH males, findings that were only partly normalized by weaning to a regular chow. IHH male rats had a 10-fold increase in serum corticosterone levels. IHH female rats had increased adiposity and serum triglycerides. We conclude that IUGR combined with an HFD throughout life increased adiposity, glucocorticoids and triglycerides in a sex-specific manner. Our data suggest that one mechanism through which the perinatal environment programs increased adiposity in IHH male rats may be via increased systemic glucocorticoids.
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White, Christy L., Megan N. Purpera, and Christopher D. Morrison. "Maternal obesity is necessary for programming effect of high-fat diet on offspring." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 5 (2009): R1464—R1472. http://dx.doi.org/10.1152/ajpregu.91015.2008.
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We tested the hypothesis that maternal consumption of dietary fat, independent from obesity, increases serum leptin in neonatal pups and predisposes them to adult obesity. Female rats either were fed a high-fat (HF) diet or a low-fat (LF) diet or were fed the HF diet but pair fed (PF) to the caloric intake of the LF group for 4 wk before breeding and throughout gestation and lactation. Dams consuming the HF diet had increased adiposity and were hyperphagic. At weaning, pups born to obese dams had significantly higher body fat and serum leptin levels and reduced insulin tolerance compared with offspring of LF-fed dams. Pups were weaned onto a chow diet until 8 wk of age, when they were then fed either HF or LF diet. At 18 wk of age, offspring from obese HF dams weighed more than offspring from nonobese LF or PF dams, and offspring eating HF diet weighed significantly more than those eating LF diet. Consequently, HF-fed offspring of obese HF dams weighed the most and LF-fed offspring from obese HF dams were similar in weight to HF-fed offspring from nonobese LF dams. These data suggest that maternal obesity exerts an independent effect on offspring body weight that is of similar magnitude as the effect of the offspring's adult diet. Furthermore, there was no difference in body weight between the nonobese LF and PF offspring on either diet. Together, these data suggest that maternal adiposity, and not dietary fat per se, induces hyperleptinemia and insulin resistance in offspring, as well as an increased body weight that persists into adulthood.
Dissertations / Theses on the topic "Offspring adiposity"
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Henderson, Amanda Marie. "Maternal B-vitamin status during development and programming of adult offspring adiposity." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61276.
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Developmental programming suggests that perinatal environmental conditions can impact risk for chronic diseases. Population studies have reported greater insulin resistance and adiposity in offspring from mothers with adequate folate but low vitamin B12 (B12) status during pregnancy. Rodent studies have reported that these effects are sex-specific. Folate, a methyl nutrient, is metabolically linked to B12. Low B12 status, even when folate is adequate, can trap folate in a metabolically inactive form. Folate deficiency is rare in Canada due to folic acid fortification of grains, yet one in 20 Canadians are estimated to be B12-deficient. The objective of this thesis is to determine the mechanisms underlying the relationship between maternal B-vitamin status during pregnancy and offspring adiposity and glucose homeostasis.
In vitro experiments assessed direct effects of folic acid on adipocyte energy metabolism. In 3T3-L1 adipocytes, cells treated with 1.6μM folic acid had lower (p≤0.05) mitochondrial respiration rates than cells treated with 0.16μM folic acid. Adipocytes treated with 1.6μM 5-methyltetrahydrofolate (5-MTHF), the circulating form of folate, had higher (p≤0.01) mitochondrial respiration rates than cells treated with 0.16μM 5-MTHF.
Female mice (C57BL/6J) were fed one of three maternal diets six weeks prior to breeding and through pregnancy/lactation: control (M-CON), supplemental folic acid with adequate B12 (SFA+B12), or SFA without B12 (SFA-B12). One male and one female from each dam were weaned onto either a control or western diet (45% kcal fat). Sex-specific differences by maternal diet were observed in the offspring. Female control-fed SFA-B12 offspring had lower (p≤0.05) serum IGF-1 (insulin-like growth factor-1) concentrations than M-CON and SFA+B12 offspring. This was accompanied by higher (p≤0.05) hepatic Cpt1a mRNA in SFA-B12 and SFA+B12 offspring than M-CON offspring. Female western-fed SFA+B12 offspring had higher (p≤0.05) hepatic FADS2 and ELOVL2 protein than M-CON offspring. Conversely, male control-fed SFA-B12 offspring had higher (p≤0.05) hepatic linoleic acid (C18:2n-6) and lower (p≤0.05) eicosapentaenoic acid (C20:5n-3) concentrations, and lower (p=0.08) hepatic ELOVL2 protein than M-CON offspring.
These findings suggest programming of offspring adiposity and glucose homeostasis by maternal B-vitamin status occurs through sex-specific alterations in IGF-1, and adipose tissue and hepatic lipid metabolism.<br>Medicine, Faculty of<br>Pathology and Laboratory Medicine, Department of<br>Graduate
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Solé, Navais Pol. "Prenatal one carbon metabolism and in utero programming of growth and adiposity in the offspringPrenatal one carbon metabolism and in utero programming of growth and adiposity in the offspring." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/401551.
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El metabolisme monocarbonat influeix positivament la salut en estadis primerencs i tardans de la vida (e.g. reducció en la prevalença de defectes del tub neural i la mort per accidents vasculars cerebrals després de la fortificació amb àcid fòlic). Tot i això, es desconeixen els efectes que el metabolisme monocarbonat in utero pot tenir sobre el creixement postnatal. S’han atribuït efectes adversos a estats elevats de folat. L’objectiu era avaluar les interaccions entre el folat i cobalamina prenatals i els seus efectes durant l’embaràs i sobre el creixement i adipositat en la descendència. Es van estudiar 563 dones del Reus-Tarragona Birth Cohort durant l’embaràs i 162 nens fins als 7.5 anys. L’estat en folats no va modificar l’associació entre l’estat inadequat en cobalamin i marcadors metabòlics i hematològics durant l’embaràs. Un estat inadequat a l’inici de l’embaràs en folat eritrocitàri, cobalamina o tHcy es va associar amb menor alçada en la descendència. Un estat inadequat en holoTC es va associar amb major IMC en la descendència. Els polimorfismes materns MTHFR 677C>T i TCN2 776C>T es van associar amb major i menor IMC i alçada en la descendència des del naixement fins als 7.5 anys respectivament. El polimorfisme MTRR 66A>G del nen es relacionava amb menor alçada i pes. Aquests resultats avalen la seguretat d’elevades concentracions de folat plasmàtic i sustenten el paper del metabolisme monocarbonat prenatal en el creixement i adipositat postnatals.<br>El metabolismo monocarbonado influye positivamente la salud en estadios tempranos y tardíos de la vida (e.g. reducción en la prevalencia de defectos del tubo neural y la muerte por accidente vascular cerebral después de la fortificación con ácido fólico). Se desconocen los efectos del metabolismo monocarbonado in utero en el crecimiento postnatal. Se han atribuido efectos adversos a un estado elevado en folato. El objetivo fue evaluar las interacciones entre el folato y cobalamina prenatales i sus efectos durante el embarazo y sobre el crecimiento y adiposidad en la progenie. Se estudiaron 563 mujeres del Reus-Tarragona Birth Cohort durante el embarazo y 162 descendientes hasta los 7.5 años de edad. Un estado elevado en folatos no modificó la asociación entre concentraciones inadecuadas de cobalamina y sus marcadores metabólicos o hematológicos durante el embarazo. Un estado inadecuado al inicio del embarazo en folato eritrocitario, cobalamina o tHcy al inicio del embarazo se asoció con menor estatura en la descendencia. Un estado inadecuado en holoTC se asoció con mayor IMC en los descendientes. Los polimorfismos maternos MTHFR 677C>T y TCN2 776C>T se asociaron con mayor y menor IMC y estatura desde el nacimiento hasta la infancia respectivamente. El polimorfismo MTRR 66A>G del niño se relacionaba con menor talla y peso. Estos resultados avalan la seguridad de concentraciones elevadas en folato plasmático y sostienen el papel del metabolismo monocarbonado prenatal en el crecimiento y adiposidad postnatales.<br>One carbon metabolism positively influences health in early and late stages of life (e.g. folic acid fortification reduced neural tube defect prevalence, homocysteine in adults and possiblystroke mortality). Whether the effects of in utero one carbon metabolism affect postnatal growth is unknown. Harmful effects of elevated folate status have been reported. We evaluated the interactions between prenatal folate and cobalamin and their effects during pregnancy and on offspring growth and adiposity at mid-childhood. 563 women from the Reus-Tarragona Birth Cohort were followed-up throughout pregnancy and 162 of their offspring until mid-childhood, when growth and adiposity were measured. Folate status did not modify the association between inadequate cobalamin and its metabolic or haematological indicators. Early pregnancy inadequate RBC folate, cobalamin or tHcy were associated with lower offspring height. Inadequate holoTC was also associated with higher offspring BMI. Maternal MTHFR 677C>T and TCN2 776C>T genetic variants were associated with higher and lower offspring BMI and height from birth to mid-childhood, respectively. Child MTRR 66A>G was associated with lower linear and ponderal growth. This endorses the safety of elevated folate status, and supports a role for prenatal one carbon metabolism on postnatal growth and adiposity.
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Pitchika, Anitha [Verfasser], Till [Gutachter] Ittermann, and Wolfgang [Gutachter] Rathmann. "Epidemiology of diabetic disorders and its long-term impact on adiposity in the offspring / Anitha Pitchika ; Gutachter: Till Ittermann, Wolfgang Rathmann." Greifswald : Universität Greifswald, 2021. http://d-nb.info/1239249721/34.
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West, J., D. A. Lawlor, L. Fairley, et al. "UK-born Pakistani-origin infants are relatively more adipose than white British infants: findings from 8704 mother-offspring pairs in the Born-in-Bradford prospective birth cohort." 2013. http://hdl.handle.net/10454/6232.
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BACKGROUND: Previous studies have shown markedly lower birth weight among infants of South Asian origin compared with those of White European origin. Whether such differences mask greater adiposity in South Asian infants and whether they persist across generations in contemporary UK populations is unclear. Our aim was to compare birth weight, skinfold thickness and cord leptin between Pakistani and White British infants and to investigate the explanatory factors, including parental and grandparental birthplace. METHODS: We examined the differences in birth weight and skinfold thickness between 4649 Pakistani and 4055 White British infants born at term in the same UK maternity unit and compared cord leptin in a subgroup of 775 Pakistani and 612 White British infants. RESULTS: Pakistani infants were lighter (adjusted mean difference -234 g 95% CI -258 to -210) and were smaller in both subscapular and triceps skinfold measurements. The differences for subscapular and triceps skinfold thickness (mean z-score difference -0.27 95% CI -0.34 to -0.20 and -0.23 95% CI -0.30 to -0.16, respectively) were smaller than the difference in birth weight (mean z-score difference -0.52 95% CI -0.58 to -0.47) and attenuated to the null with adjustment for birth weight (0.03 95% CI -0.03 to 0.09 and -0.01 95% CI -0.08 to 0.05, respectively). Cord leptin concentration (indicator of fat mass) was similar in Pakistani and White British infants without adjustment for birth weight, but with adjustment became 30% higher (95% CI 17% to 44%) among Pakistani infants compared with White British infants. The magnitudes of difference did not differ by generation. CONCLUSIONS: Despite being markedly lighter, Pakistani infants had similar skinfold thicknesses and greater total fat mass, as indicated by cord leptin, for a given birth weight than White British infants. Any efforts to reduce ethnic inequalities in birth weight need to consider differences in adiposity and the possibility that increasing birth weight in South Asian infants might inadvertently worsen health by increasing relative adiposity.
Books on the topic "Offspring adiposity"
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Macronutrients and fibre requirements during pregnancy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0004.
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In this chapter, the impact of varying intakes of protein, carbohydrate and lipids, which are the key nutrients that contribute to calorie intake, is examined. Fibre is also an important food component that needs to be considered. The maternal macronutrient profile can influence embryonic and fetal development. For instance, both low and excessively high protein intakes during pregnancy are associated with restricted growth, increased adiposity, and impaired glucose tolerance. High-fat maternal diets can significantly increase the susceptibility to diet-induced obesity and percentage total body fat in offspring, although types of fats need to be considered, as intake of polyunsaturated fatty acids is important for fetal development. The type and content of carbohydrate (high- vs low-glycaemic sources) in the maternal diet influences blood glucose concentration, which has a direct effect on fetal glucose levels and metabolism.
Book chapters on the topic "Offspring adiposity"
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de Fátima Leão, Valéria, Juliana Montani Raimundo, Letícia Lima Dias Moreira Ferreira, et al. "Effects of Paternal Hypothalamic Obesity and Taurine Supplementation on Adiposity and Vascular Reactivity in Rat Offspring." In Taurine 9. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15126-7_60.
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Jevtovic, Filip, and Linda May. "Influence of Maternal Exercise on Maternal and Offspring Metabolic Outcomes." In Maternal and Child Health [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106566.
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Epigenetic transmission of metabolic disease to an offspring increases their risk for development of metabolic disease later in life. With the increasing rates of obesity in women of child-bearing age it is critical to develop strategies to prevent perpetuating metabolic disease across generations. Maternal exercise during gestation imprints offspring metabolic phenotype, thus increasing their imperviousness to metabolic assaults later in life. In rodent models, maternal exercise before and during gestation leads to enhanced offspring glycemic control, mitochondrial bioenergetics, and lower adiposity, which decreases their risk for development of future metabolic disease. In humans, maternal gestational exercise decreases pregnancy complications and improves maternal and offspring metabolism on both the whole-body and the cellular level. Maternal exercise restores the obesity-induced metabolic derangements, restoring maternal and offspring metabolic phenotype. While unknown, different exercise modalities might have a differential effect, however, evidence remains scarce.
Conference papers on the topic "Offspring adiposity"
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Pitchika, Anitha, Manja Jolink, Christiane Winkler, et al. "5 Associations of maternal type 1 diabetes with childhood adiposity and metabolic health in the offspring." In ISEE Young 2018, Early Career Researchers Conference on Environmental Epidemiology – Together for a Healthy Environment, 19–20 March 2018, Freising, Germany. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-iseeabstracts.65.
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Bruder, Johanna, Mersiha Hasic, and Martin Klingenspor. "Maternal Housing Temperature and Diet – Programming Effects on Browning Capacity in Female and Male Offspring (#59)." In Abstracts des Adipositas-Kongresses 2022 zur 38. Jahrestagung der Deutschen Adipositas Gesellschaft e.V. DAG. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1755680.
Full textReports on the topic "Offspring adiposity"
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Gao, Hui, Ya-fei Wang, Zi-wei Wang, and Yue Wang. Prenatal phthalate exposure is associated with age-specific alterations in markers of adiposity in offspring: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.7.0090.
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