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Journal articles on the topic 'Fetal adiposity'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Farah, Nadine, Jennifer Hogan, Vicky O'Dwyer, Bernard Stuart, Mairead Kennelly, and Michael J. Turner. "Influence of Maternal Glycemia on Intrauterine Fetal Adiposity Distribution after a Normal Oral Glucose Tolerance Test at 28 Weeks Gestation." Experimental Diabetes Research 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/951203.

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Objective. To examine the relationship between maternal glucose levels and intrauterine fetal adiposity distribution in women with a normal oral glucose tolerance test (OGTT) at 28 weeks gestation.Study Design. We recruited 231 women with a singleton pregnancy. At 28 and 37 weeks gestation, sonographic measurements of fetal body composition were performed. Multiple regression analysis was used to study the influence of different maternal variables on fetal adiposity distribution.Results. Maternal glucose levels correlated with the fetal abdominal subcutaneous tissue measurements (; ) and with birth weight (; ). Maternal glucose levels did not correlate with the fetal mid-thigh muscle thickness and mid-thigh subcutaneous tissue measurements.Conclusion. We found that in nondiabetic women maternal glucose levels not only influence fetal adiposity and birth weight, but also influence the distribution of fetal adiposity. This supports previous evidence that maternal glycemia is a key determinant of intrauterine fetal programming.

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2

Franca Neto, Antonio H., Melania M. Amorim, Adriana S. Melo, Maria do Carmo P. Lima, Aline Sena, and Lívia Dantas. "Accumulation of Adiposity Fetal During Pregnancy." Obstetrics & Gynecology 127 (May 2016): 132S—133S. http://dx.doi.org/10.1097/01.aog.0000483535.48712.39.

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3

Franca Neto, Antonio H., Melania M. Amorim, Adriana S. Melo, Aline Sena, Maria do Carmo P. Lima, and Jamila V. Silva. "Thigh Measurement and Adiposity Fetal Accumulation." Obstetrics & Gynecology 127 (May 2016): 149S. http://dx.doi.org/10.1097/01.aog.0000483595.55443.9d.

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4

Vega-Sanchez, Rodrigo, Hector A. Barajas-Vega, Guadalupe Rozada, Aurora Espejel-Nuñez, Jorge Beltran-Montoya, and Felipe Vadillo-Ortega. "Association between adiposity and inflammatory markers in maternal and fetal blood in a group of Mexican pregnant women." British Journal of Nutrition 104, no. 12 (July 23, 2010): 1735–39. http://dx.doi.org/10.1017/s0007114510002825.

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In the present pilot study, we evaluated the effect of maternal adiposity on the plasma concentration of adipocytokines in pregnant women and their newborns. Twenty patients with term gestations without labour were initially selected by pregestational BMI and then classified into two study groups (n 10 each), according to their median value of adiposity (total body fat). Concentrations of TNF-α, IL-1β, IL-6, leptin and adiponectin in plasma of maternal peripheral blood and fetal cord blood were measured and correlated to maternal adiposity. Maternal adiposity showed a significant negative correlation with fetal adiponectin (r − 0·587, P = 0·01) and IL-6 (r − 0·466, P = 0·05), a significant positive correlation with maternal leptin (r 0·527, P = 0·02) and no correlation with TNF-α or IL-1β. Adiponectin was higher in fetal plasma than in maternal plasma (P = 0·043), but significantly lower in newborns from women with high adiposity than in newborns from women with low adiposity (P = 0·040). Our results suggest that fetuses from obese women may be less able to control inflammation, due to lower circulating anti-inflammatory adipocytokines, which could limit their optimal development or even increase the risk of abortion or preterm labour.

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5

Sena, Aline Silva Santos, Alex Sandro Rolland de Souza, Vivianne de Oliveira Barros, Maria do Carmo Pinto Lima, Adriana Suely Oliveira Melo, and Melania Maria Ramos de Amorim. "Prenatal factors associated with fetal visceral adiposity." Jornal de Pediatria 96, no. 3 (May 2020): 341–49. http://dx.doi.org/10.1016/j.jped.2018.11.013.

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6

Sena, Aline Silva Santos, Alex Sandro Rolland de Souza, Vivianne de Oliveira Barros, Maria do Carmo Pinto Lima, Adriana Suely Oliveira Melo, and Melania Maria Ramos de Amorim. "Prenatal factors associated with fetal visceral adiposity." Jornal de Pediatria (Versão em Português) 96, no. 3 (May 2020): 341–49. http://dx.doi.org/10.1016/j.jpedp.2018.11.025.

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7

Jarvie, Eleanor M., Frances M. Stewart, Jane E. Ramsay, E. Ann Brown, Barbara J. Meyer, Gunilla Olivecrona, Bruce A. Griffin, and Dilys J. Freeman. "Maternal Adipose Tissue Expansion, A Missing Link in the Prediction of Birth Weight Centile." Journal of Clinical Endocrinology & Metabolism 105, no. 3 (December 13, 2019): e814-e825. http://dx.doi.org/10.1210/clinem/dgz248.

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Abstract Context Maternal body mass index (BMI) is associated with increased birth weight but does not explain all the variance in fetal adiposity. Objective To assess the contribution of maternal body fat distribution to offspring birth weight and adiposity. Design Longitudinal study throughout gestation and at delivery. Setting Women recruited at 12 weeks of gestation and followed up at 26 and 36 weeks. Cord blood was collected at delivery. Patients Pregnant women (n = 45) with BMI 18.0 to 46.3 kg/m2 and healthy pregnancy outcome. Methods Maternal first trimester abdominal subcutaneous and visceral adipose tissue thickness (SAT and VAT) was assessed by ultrasound. Main Outcome Measures Maternal body fat distribution, maternal and cord plasma glucose and lipid concentrations, placental weight, birth weight, and fetal adiposity assessed by cord blood leptin. Results VAT was the only anthropometric measure independently associated with birth weight centile (r2 adjusted 15.8%, P = .002). BMI was associated with trimester 2 and trimesters 1 through 3 area under the curve (AUC) glucose and insulin resistance (Homeostatic Model Assessment). SAT alone predicted trimester 2 lipoprotein lipase (LPL) mass (a marker of adipocyte insulin sensitivity) (11.3%, P = .017). VAT was associated with fetal triglyceride (9.3%, P = .047). Placental weight was the only independent predictor of fetal adiposity (48%, P < .001). Maternal trimester 2 and AUC LPL were inversely associated with fetal adiposity (r = -0.69, P = .001 and r = -0.58, P = .006, respectively). Conclusions Maternal VAT provides additional information to BMI for prediction of birth weight. VAT may be a marker of reduced SAT expansion and increased availability of maternal fatty acids for placental transport.

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8

Luo, Z.-C., A.-M. Nuyt, E. Delvin, F. Audibert, I. Girard, B. Shatenstein, E. Levy, P. Julien, and W. D. Fraser. "Understanding parental anthropometrical, maternal, and fetal metabolic determinants of fetal adiposity." Canadian Journal of Diabetes 35, no. 2 (January 2011): 177. http://dx.doi.org/10.1016/s1499-2671(11)52143-4.

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9

Edwards, L. J., J. R. McFarlane, K. G. Kauter, and I. C. McMillen. "Impact of periconceptional nutrition on maternal and fetal leptin and fetal adiposity in singleton and twin pregnancies." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 1 (January 2005): R39—R45. http://dx.doi.org/10.1152/ajpregu.00127.2004.

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It has been proposed that maternal nutrient restriction may alter the functional development of the adipocyte and the synthesis and secretion of the adipocyte-derived hormone, leptin, before birth. We have investigated the effects of restricted periconceptional undernutrition and/or restricted gestational nutrition on fetal plasma leptin concentrations and fetal adiposity in late gestation. There was no effect of either restricted periconceptional or gestational nutrition on maternal or fetal plasma leptin concentrations in singleton or twin pregnancies during late gestation. In ewes carrying twins, but not singletons, maternal plasma leptin concentrations in late gestation were directly related to the change in ewe weight that occurred during the 60 days before mating [maternal leptin = 0.9 (change in ewe weight) + 7.8; r = 0.6, P < 0.05]. In twin, but not singleton, pregnancies, there was also a significant relationship between maternal and fetal leptin concentrations (maternal leptin = 0.5 fetal leptin + 4.2, r = 0.63, P < 0.005). The relative mass of perirenal fat was also significantly increased in twin fetal sheep in the control-restricted group (6.0 ± 0.5) compared with the other nutritional groups (control-control: 4.1 ± 0.4; restricted-restricted: 4.4 ± 0.4; restricted-control: 4.3 ± 0.3). In conclusion, the impact of maternal undernutrition on maternal plasma leptin concentrations during late gestation is dependent on fetal number. Furthermore, we have found that there is an increased fetal adiposity in the twins of ewes that experienced restricted nutrition throughout gestation, and this may be important in the programming of postnatal adiposity.

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10

Wallace, Jacqueline M., John S. Milne, Clare L. Adam, and Raymond P. Aitken. "Impact of donor and recipient adiposity on placental and fetal growth in adolescent sheep." Reproduction 153, no. 4 (April 2017): 381–94. http://dx.doi.org/10.1530/rep-16-0590.

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The influence of maternal obesity during oocyte development and its putative interaction with nutrient reserves at conception on pregnancy outcome were examined in an adolescent sheep model. Donor ewes were nutritionally managed to achieve contrasting adiposity (control (CD)/obese (ObD)) for 6 weeks prior to superovulation and inseminated by a non-obese sire. Morulae from 6 CD and 7 ObD were transferred in singleton into adolescent recipients of identical age but differing adiposity, classified as relatively fat or thin respectively. Thereafter, all were overnourished to promote rapid growth/adiposity (2 × 2 design, 13/14 pregnancies/group). A fifth recipient group of intermediate adiposity received embryos from another 5 CD, was offered a moderate intake to maintain adiposity throughout gestation and acted as controls for normal pregnancy outcome (optimally treated control (OTC), 19 pregnancies). Donor obesity did not influence ovulation, fertilisation or recovery rates or impact embryo morphology. Gestation length and colostrum yield were unaffected by donor or recipient adiposity and were reduced relative to OTC. Total fetal cotyledon and lamb birth weights were independent of initial donor adiposity but reduced in relatively thin vs relatively fat recipients and lower than those in the OTC group. In spite of high placental efficiency, the incidence of fetal growth restriction was greatest in the thin recipients. Thus, maternal adiposity at conception, but not pre-conception maternal obesity, modestly influences the feto-placental growth trajectory, whereas comparison with the OTC indicates that high gestational intakes to promote rapid maternal growth remain the dominant negative influence on pregnancy outcome in young adolescents. These findings inform dietary advice for pregnant adolescent girls.

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11

Athar, Sufia, and Amna Khalifa Tellisi. "Fetal Growth Disorders and Influence of Maternal Adiposity." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A12—A13. http://dx.doi.org/10.1210/jendso/bvab048.022.

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Abstract Introduction: Infant birth weight is recognized as the leading indicator of health among infants and affects a wide range of subsequent outcomes later in life. The incidence of neonates with high birth weight has increased in recent years. Many studies in the past have revealed that high birth weight is associated with neonatal morbidity and mortality and associated with complications in later life. These complications include shoulder dystocia, birth trauma, asphyxia, and neonatal deaths. In the later life these neonates have high risk for obesity, hypertension, diabetes mellitus and cancer. High pre-pregnancy body mass index (BMI) has been reported as a well-established risk factors for adverse pregnancy outcomes. Despite the high prevalence of maternal obesity in the gulf region, only a few studies in this regard have been published. Methods: A retrospective service evaluation was conducted at a secondary hospital to evaluate the effect of pre-pregnancy BMI on neonatal birth weight. 950 women were randomly selected from women delivered at or more than 37 weeks gestation and grouped on the basis of pregnancy BMI as group A-BMI 18.5–24.9 kg/m2, group-B- BMI 25–29.9 kg/m2 and group C-BMI >30 kg/m2. Infants were grouped according to birth weight as low birth weight(<2500 g), normal birth weight (2500–3999 g), and high birth weight >4000g and correlation was studied with maternal body mass index. Chi square test was used for statistical evaluation using Medcal online software. Results: In the study group, 34.43% women had normal body mass index, 37.21 % women were overweight and 28.36 % were obese. In group A, 6.50% and 4.64 % infants were with low and high birth weight, respectively. In group B, 4.3% and 5.73 % were with low and high birth weight, respectively. In group C, 4.51% and 20.33 % infants were with low and high birth weight, respectively. In comparison to women with normal BMI, low birth weight infants in group B (OR-0.922, 95% CI- 0.327–1.275) and group C (OR- 0.679, 95% CI-0.682–1.572) were not statistically significant. High birth weight infants in group B (OR- 1.2482, 95% CI- 0.3270 to 1.2756, p = 0.2080) and group C (OR-5.230, 95% CI-2.875–9.512, p= < 0.0001) were positively correlated with pre-pregnancy BMI. Pre-pregnancy overweight and obesity increased the risk of high birth weight (OR- 1.248 and 5.230 respectively). The results were statistically significant in obese women (p=< 0.0001). Conclusion: Women with pre-pregnancy overweight and obesity have higher likelihood of high birth weight in infants. Pre-pregnancy weight loss is the key to reduce maternal and fetal complications. Early pregnancy booking and antenatal fetal surveillance is recommended for all women with high body mass index.

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12

Mastorakos, George, Dimosthenis Maliopoulos, Spyridoula Kasioni, Alexandra Bargiota, Thomas M. Barber, Chrysanthi Skevaki, Ioannis Papassotiriou, et al. "Relationship Between Maternal Bone Biomarkers and Fetal Adiposity Through Normal Pregnancy." Journal of Clinical Endocrinology & Metabolism 106, no. 7 (March 12, 2021): e2647-e2655. http://dx.doi.org/10.1210/clinem/dgab152.

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Abstract Purpose To examine the association of maternal bone markers [sclerostin, soluble receptor activator of nuclear factor-κB ligand (sRANKL), osteocalcin, 25-hydroxyvitamin D3] with fetal intra-abdominal and subcutaneous adipose tissue deposition and birthweight during normal pregnancy. Methods One hundred pregnant women (aged 30.4 ± 5.6 years, mean ± SD) with prepregnancy body mass index = 24.1 ± 4.6 kg/m2 were seen prospectively during each trimester. At each visit they were submitted to anthropometric measurements, a fasting blood sampling, a 75-g oral glucose tolerance test, and a fetal ultrasonogram. At birth, neonates had birth weight measurement. Results In the second trimester, maternal sclerostin concentrations correlated positively with fetal abdominal circumference and birth weight; maternal sRANKL concentrations correlated positively with fetal abdominal subcutaneous fat thickness, sagittal abdominal diameter, and abdominal circumference. Fetuses born to mothers with greater (>254 ng/mL), compared to fetuses born to mothers with lower (≤254ng/mL), sRANKL concentrations had greater abdominal circumference, sagittal diameter, and abdominal subcutaneous fat thickness. Maternal serum sclerostin concentrations were the best positive predictors of birth weight. In the third trimester maternal sclerostin concentrations correlated positively with fetal sagittal abdominal diameter; maternal sRANKL concentrations positively correlated with fetal abdominal circumference and fetal abdominal sagittal diameter. Conclusions Maternal bone markers sclerostin and sRANKL may relate to fetal intra-abdominal adipose tissue deposition through as yet unknown direct or indirect mechanisms, thus contributing to birthweight.

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13

Chawla, R., D. R. McCance, S. McKenna, I. S. Young, C. C. Patterson, J. Rangarajan, A. C. Reisetter, et al. "The chromosome 3q25 locus associated with fetal adiposity is not associated with childhood adiposity." Nutrition & Diabetes 4, no. 9 (September 2014): e138-e138. http://dx.doi.org/10.1038/nutd.2014.35.

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14

Walsh, Jennifer, Mark Kilbane, Rhona Mahony, Michael Foley, Malachi McKenna, and Fionnuala McAuliffe. "236: Impact of maternal and fetal adiposity on maternal and fetal vitamin D." American Journal of Obstetrics and Gynecology 206, no. 1 (January 2012): S115. http://dx.doi.org/10.1016/j.ajog.2011.10.254.

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15

Walsh, Jennifer M., Rhona Mahony, Jacinta Byrne, Michael Foley, and Fionnuala M. McAuliffe. "The association of maternal and fetal glucose homeostasis with fetal adiposity and birthweight." European Journal of Obstetrics & Gynecology and Reproductive Biology 159, no. 2 (December 2011): 338–41. http://dx.doi.org/10.1016/j.ejogrb.2011.09.022.

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16

Lapiedra, M. Zamora, M. Comas Rovira, C. L. Heredia, A. Moreno Baró, L. Martí Malgosa, and B. Cochs Cosme. "VP34.04: Maternal obesity and fetal adiposity: a cohort study." Ultrasound in Obstetrics & Gynecology 58, S1 (October 2021): 89–312. http://dx.doi.org/10.1002/uog.24520.

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17

Radaelli, Tatjana, Jennifer Uvena-Celebrezze, Judi Minium, Larraine Huston-Presley, Patrick Catalano, and Sylvie Hauguel-de Mouzon. "Maternal Interleukin-6: Marker of Fetal Growth and Adiposity." Journal of the Society for Gynecologic Investigation 13, no. 1 (January 2006): 53–57. http://dx.doi.org/10.1016/j.jsgi.2005.10.003.

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18

Walsh, JM, RM Mahony, ME Foley, and FM McAuliffe. "Leptin: a biomarker of fetal adiposity and insulin resistance." Archives of Disease in Childhood - Fetal and Neonatal Edition 97, Suppl 1 (April 2012): A108.2—A108. http://dx.doi.org/10.1136/fetalneonatal-2012-301809.353.

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19

Sarr, Ousseynou, Kaiping Yang, and Timothy R. H. Regnault. "In UteroProgramming of Later Adiposity: The Role of Fetal Growth Restriction." Journal of Pregnancy 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/134758.

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Intrauterine growth restriction (IUGR) is strongly associated with obesity in adult life. The mechanisms contributing to the onset of IUGR-associated adult obesity have been studied in animal models and humans, where changes in fetal adipose tissue development, hormone levels and epigenome have been identified as principal areas of alteration leading to later life obesity. Following an adversein uterodevelopment, IUGR fetuses display increased lipogenic and adipogenic capacity in adipocytes, hypoleptinemia, altered glucocorticoid signalling, and chromatin remodelling, which subsequently all contribute to an increased later life obesity risk. Data suggest that many of these changes result from an enhanced activity of the adipose master transcription factor regulator, peroxisome proliferator-activated receptor-γ(PPARγ) and its coregulators, increased lipogenic fatty acid synthase (FAS) expression and activity, and upregulation of glycolysis in fetal adipose tissue. Increased expression of fetal hypothalamic neuropeptide Y (NPY), altered hypothalamic leptin receptor expression and partitioning, reduced adipose noradrenergic sympathetic innervations, enhanced adipose glucocorticoid action, and modifications in methylation status in the promoter of hepatic and adipose adipogenic and lipogenic genes in the fetus also contribute to obesity following IUGR. Therefore, interventions that inhibit these fetal developmental changes will be beneficial for modulation of adult body fat accumulation.

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Rebholz, Sandra L., Katie T. Burke, Qing Yang, Patrick Tso, and Laura A. Woollett. "Dietary fat impacts fetal growth and metabolism: uptake of chylomicron remnant core lipids by the placenta." American Journal of Physiology-Endocrinology and Metabolism 301, no. 2 (August 2011): E416—E425. http://dx.doi.org/10.1152/ajpendo.00619.2010.

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The fetus requires significant energy for growth and development. Although glucose is a major source of energy for the fetus, other maternal nutrients also appear to promote growth. Thus, the goal of these studies was to determine whether triglyceride-rich remnants are taken up by the placenta and whether maternal dietary lipids, independently of adiposity, can impact fetal growth. To accomplish our first goal, chylomicron particles were duallly labeled with cholesteryl ester and triglycerides. The placenta took up remnant particles/core lipids at rates greater than adipose tissue and skeletal muscle but less than the liver. Although the placenta expresses apoE receptors, uptake of chylomicron remnants and/or core lipids can occur independently of apoE. To determine the impact of dietary lipid on fetal growth, independent of maternal adiposity, females were fed high-fat diets (HFD) for 1 mo; there was no change in adiposity or leptin levels prior to or during pregnancy of dams fed HFD. Fetal masses were greater in dams fed HFD, and mRNA levels of proteins involved in fatty acid oxidation (CPT I, PPARα), but not glucose oxidation (pyruvate kinase) or other regulatory processes (HNF-4α, LXR), were increased with maternal dietary fat. There was also no change in mRNA levels of proteins involved in placental glucose and fatty acid transport, and GLUT1 protein levels in microvillous membranes were similar in placentas of dams fed either diet. Thus, the ability of the placenta to take up chylomicron remnant core lipids likely contributes to accelerated fetal growth in females fed high fat diets.

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Antony, Kathleen, Dianne Glass, Emily Steinbis, Diana Racusin, Najma Aijiz, and Kjersti Aagaard. "2074928 Determining Fetal Adiposity in Utero Based on Sonographic Measurements of Fetal Buoyancy (Rate of Fetal Rise, RFR)." Ultrasound in Medicine & Biology 41, no. 4 (April 2015): S42. http://dx.doi.org/10.1016/j.ultrasmedbio.2014.12.199.

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Antony, Kathleen, Dianne Glass, Emily Steinbis, Diana Racusin, Najma Aijiz, and Kjersti Aagaard. "494: Determining fetal adiposity in utero based on sonographic measurements of fetal buoyancy (rate of fetal rise, RFR)." American Journal of Obstetrics and Gynecology 212, no. 1 (January 2015): S249—S250. http://dx.doi.org/10.1016/j.ajog.2014.10.540.

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23

Mele, James, Sribalasubashini Muralimanoharan, Alina Maloyan, and Leslie Myatt. "Impaired mitochondrial function in human placenta with increased maternal adiposity." American Journal of Physiology-Endocrinology and Metabolism 307, no. 5 (September 1, 2014): E419—E425. http://dx.doi.org/10.1152/ajpendo.00025.2014.

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The placenta plays a key role in regulation of fetal growth and development and in mediating in utero developmental programming. Obesity, which is associated with chronic inflammation and mitochondrial dysfunction in many tissues, exerts a programming effect in pregnancy. We determined the effect of increasing maternal adiposity and of fetal sex on placental ATP generation, mitochondrial biogenesis, expression of electron transport chain subunits, and mitochondrial function in isolated trophoblasts. Placental tissue was collected from women with prepregnancy BMI ranging from 18.5 to 45 following C-section at term with no labor. Increasing maternal adiposity was associated with excessive production of reactive oxygen species and a significant reduction in placental ATP levels in placentae with male and female fetuses. To explore the potential mechanism of placental mitochondrial dysfunction, levels of transcription factors regulating the expression of genes involved in electron transport and mitochondrial biogenesis were measured. Our in vitro studies showed significant reduction in mitochondrial respiration in cultured primary trophoblasts with increasing maternal obesity along with an abnormal metabolic flexibility of these cells. This reduction in placental mitochondrial respiration in pregnancies complicated by maternal obesity could compromise placental function and potentially underlie the increased susceptibility of these pregnancies to fetal demise in late gestation and to developmental programming.

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Yajnik, C. S. "Obesity epidemic in India: intrauterine origins?" Proceedings of the Nutrition Society 63, no. 3 (August 2004): 387–96. http://dx.doi.org/10.1079/pns2004365.

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The epidemic of ‘obesity’ in India is not appreciated because BMI underestimates the adiposity of Indians. Specific adiposity measurements are necessary for recognition of the adiposity of ‘thin’ Indians. The origin of this adiposity is only beginning to be understood. In addition to a possible genetic predisposition, intrauterine ‘programming’ might be responsible, although in the ‘thrifty phenotype’ hypothesis the adiposity of the ‘thin’ fetus has not been appreciated. Dutch men who faced ‘winter hunger’ during the first trimester of their in utero life have become more obese as adults. Low birth weight predicts central obesity in some studies, including studies in urban children. It has also been shown that small and thin Indian newborns (weight 2·7?kg and ponderal index 2·4?kg\m3) have poor muscle and visceral mass but higher adiposity for a given weight compared with white Caucasian babies. This body composition is influenced by maternal adiposity before pregnancy and by aspects of maternal nutritional intake and circulating nutrient concentrations during pregnancy. There are no strong paternal determinants of adiposity at birth. Adiposity may be an integral part of the orchestrated adjustments made to support ‘brain preservation’ during intrauterine growth, because brain tissue is predominantly fat. Increased nutrition in the face of a genetic predisposition or multigenerational undernutrition increases maternal insulin resistance in late pregnancy and promotes fetal adiposity even in absence of marked hyperglycaemia. Further research is necessary to define the role of specific nutrients and metabolites in the intrauterine processes promoting adiposity before maternal interventions to curtail the epidemic of obesity and diabetes are planned.

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Pereira-da-Silva, L., and D. Virella. "Which type of maternal dietary polyunsaturated fat affects fetal adiposity?" Journal of Public Health 42, no. 3 (May 14, 2019): 639. http://dx.doi.org/10.1093/pubmed/fdz048.

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O'Brien, C. M., R. Grivell, A. Deussen, J. Louise, and J. Dodd. "OC02.02: Cardiometabolic biomarkers are associated with fetal overgrowth and adiposity." Ultrasound in Obstetrics & Gynecology 50 (September 2017): 3–4. http://dx.doi.org/10.1002/uog.17576.

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Hehir, M. P., N. Burke, G. Burke, M. J. Turner, F. M. Breathnach, F. M. Mcauliffe, J. J. Morrison, et al. "Sonographic markers of fetal adiposity and risk of Cesarean delivery." Ultrasound in Obstetrics & Gynecology 54, no. 3 (September 2019): 338–43. http://dx.doi.org/10.1002/uog.20263.

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28

Farah, N., V. Donnelly, M. Kennelly, B. Stuart, and M. Turner. "OP32.08: Maternal body composition as a predictor of fetal adiposity." Ultrasound in Obstetrics & Gynecology 34, S1 (September 2009): 167. http://dx.doi.org/10.1002/uog.6976.

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FERREIRA, JOSE CARLOS, SANAA CHOUFANI, JOHN KINGDOM, and ROSANNA WEKSBERG. "EPIGENETIC PROGRAMMING AND FETAL GROWTH RESTRICTIONS." Fetal and Maternal Medicine Review 21, no. 3 (June 3, 2010): 204–24. http://dx.doi.org/10.1017/s0965539510000057.

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Normal fetal growth and development depends on multiple molecular mechanisms that coordinate both placental and fetal development. Efforts to better understand fetal/placental growth dysregulation and fetal growth restriction (FGR) are now being driven by several findings that highlight the longterm impact of FGR on susceptibility to disease. The association of poor fetal growth to perinatal medical complications is well accepted but more recent data also show that FGR is linked to common, serious adult health problems. Several large-scale human epidemiological studies from diverse countries have shown that conditions such as coronary heart disease, hypertension, stroke, type 2 diabetes mellitus, adiposity, insulin resistance and osteoporosis are more prevalent in individuals with a history of low birthweight.

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Mühlhäusler, BS, CT Roberts, JR McFarlane, KG Kauter, and IC McMillen. "Leptin is a signal of adiposity in fetuses of pregnant ewes fed at or above maintenance energy requirements." Proceedings of the British Society of Animal Science 2002 (2002): 5. http://dx.doi.org/10.1017/s175275620000661x.

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In the adult, circulating leptin concentrations are dependent on body fat content and on current nutrient intake. Whilst leptin concentrations in umbilical cord blood correlate with fetal adiposity in the human neonate, it is unknown whether leptin acts as a signal of fat mass before birth or whether changes in maternal nutrient intake alter plasma leptin concentrations in the fetus. We have therefore investigated the relationship between fetal plasma leptin concentrations and fetal fat mass in pregnant ewes fed at or above maintenance energy requirements.

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Veena, Sargoor R., Ghattu V. Krishnaveni, Samuel C. Karat, Clive Osmond, and Caroline HD Fall. "Testing the fetal overnutrition hypothesis; the relationship of maternal and paternal adiposity to adiposity, insulin resistance and cardiovascular risk factors in Indian children." Public Health Nutrition 16, no. 9 (August 16, 2012): 1656–66. http://dx.doi.org/10.1017/s1368980012003795.

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AbstractObjectiveWe aimed to test the fetal overnutrition hypothesis by comparing the associations of maternal and paternal adiposity (sum of skinfolds) with adiposity and cardiovascular risk factors in children.DesignChildren from a prospective birth cohort had anthropometry, fat percentage (bio-impedance), plasma glucose, insulin and lipid concentrations and blood pressure measured at 9·5 years of age. Detailed anthropometric measurements were recorded for mothers (at 30 ± 2 weeks’ gestation) and fathers (5 years following the index pregnancy).SettingHoldsworth Memorial Hospital, Mysore, India.SubjectsChildren (n504), born to mothers with normal glucose tolerance during pregnancy.ResultsTwenty-eight per cent of mothers and 38 % of fathers were overweight/obese (BMI ≥ 25·0 kg/m2), but only 4 % of the children were overweight/obese (WHO age- and sex-specific BMI ≥ 18·2 kg/m2). The children's adiposity (BMI, sum of skinfolds, fat percentage and waist circumference), fasting insulin concentration and insulin resistance increased with increasing maternal and paternal sum of skinfolds adjusted for the child's sex, age and socio-economic status. Maternal and paternal effects were similar. The associations with fasting insulin and insulin resistance were attenuated after adjusting for the child's current adiposity.ConclusionsIn this population, both maternal and paternal adiposity equally predict adiposity and insulin resistance in the children. This suggests that shared family environment and lifestyle, or genetic/epigenetic factors, influence child adiposity. Our findings do not support the hypothesis that there is an intra-uterine overnutrition effect of maternal adiposity in non-diabetic pregnancies, although we cannot rule out such an effect in cases of extreme maternal obesity, which is rare in our population.

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Ibáñez, Lourdes, Giorgia Sebastiani, Abel Lopez-Bermejo, Marta Díaz, Maria Dolores Gómez-Roig, and Francis de Zegher. "Gender Specificity of Body Adiposity and Circulating Adiponectin, Visfatin, Insulin, and Insulin Growth Factor-I at Term Birth: Relation to Prenatal Growth." Journal of Clinical Endocrinology & Metabolism 93, no. 7 (July 1, 2008): 2774–78. http://dx.doi.org/10.1210/jc.2008-0526.

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Abstract Context: Fetal development is thought to be gender specific for adiposity and circulating insulin and IGF-I but not adipokinemia, as judged by serum visfatin and adiponectin at term birth. We studied the potential relationship between these gender specificities and fetal growth. Setting: The study was conducted at a university hospital. Study Population: Subjects included 96 strictly matched neonates born appropriate for gestational age (AGA; 24 girls, 24 boys) or small for gestational age (SGA; 24 girls, 24 boys). Main Outcomes: Outcomes included serum insulin, IGF-I, visfatin, total and high-molecular-weight (HMW) adiponectin, osteocalcin at term birth, and neonatal body composition by absorptiometry. Results: Cord insulin and IGF-I levels were higher in girls than boys (P ≤ 0.01), in both the AGA and SGA subpopulation. In AGA newborns, fat and lean mass were each gender specific (P < 0.0001), whereas visfatin and total and HMW adiponectin were not. Conversely, in SGA newborns, visfatin and HMW adiponectin were gender specific (higher levels in girls), whereas body adiposity was not. In SGA fetuses, the distribution of adiponectin isoforms was in both genders shifted toward HMW (P < 0.005 vs. AGA). Cord osteocalcin did not differ by either gender or birth weight. Conclusion: At term birth, the gender specificity of adiposity and circulating visfatin and HMW adiponectin appeared to depend on prenatal growth, whereas the gender specificity of insulin and IGF-I levels did not. The fetal shift in adiponectin isoforms may contribute to explain why SGA newborns tend to be hypersensitive to insulin.

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Ruiz-Palacios, María, Antonio José Ruiz-Alcaraz, María Sanchez-Campillo, and Elvira Larqué. "Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus." Annals of Nutrition and Metabolism 70, no. 1 (2017): 16–25. http://dx.doi.org/10.1159/000455904.

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Background: Gestational diabetes mellitus (GDM) is associated with increased fetal adiposity, which may increase the risk of obesity in adulthood. The placenta has insulin receptors and maternal insulin can activate its signaling pathways, affecting the transport of nutrients to the fetus. However, the effects of diet or insulin treatment on the placental pathophysiology of GDM are unknown. Summary: There are very few studies on possible defects in the insulin signaling pathway in the GDM placenta. Such defects could influence the placental transport of nutrients to the fetus. In this review we discuss the state of insulin signaling pathways in placentas of women with GDM, as well as the role of exogenous insulin in placental nutrient transport to the fetus, and fetal adiposity. Key Messages: Maternal insulin in the third trimester is correlated with fetal abdominal circumference at that time, suggesting the important role of insulin in this process. Since treatment with insulin at the end of pregnancy may activate placental nutrient transport to the fetus and promote placental fatty acid transfer, it would be interesting to improve maternal hyperlipidemia control in GDM subjects treated with this hormone. More research in this area with high number of subjects is necessary.

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Symonds, Michael E., Sarah Pearce, Jayson Bispham, David S. Gardner, and Terence Stephenson. "Timing of nutrient restriction and programming of fetal adipose tissue development." Proceedings of the Nutrition Society 63, no. 3 (August 2004): 397–403. http://dx.doi.org/10.1079/pns2004366.

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It is apparent from epidemiological studies that the timing of maternal nutrient restriction has a major influence on outcome in terms of predisposing the resulting offspring to adult obesity. The present review will consider the extent to which maternal age, parity and nutritional restriction at defined stages of gestation can have important effects on fat deposition and endocrine sensitivity of adipose tissue in the offspring. For example, in 1-year-old sheep the offspring of juvenile mothers have substantially reduced fat deposition compared with those born to adult mothers. Offspring of primiparous adult mothers, however, show increased adiposity compared with those born to multiparous mothers. These offspring of multiparous ewes show retained abundance of the brown adipose tissue-specific uncoupling protein 1 at 1 month of age. A stimulated rate of metabolism in brown fat of these offspring may act to reduce adipose tissue deposition in later life. In terms of defined windows of development that can programme adipose tissue growth, maternal nutrient restriction targetted over the period of maximal placental growth results in increased adiposity at term in conjunction with enhanced abundance of mRNA for the insulin-like growth factor-I and -II receptors. In contrast, nutrient restriction in late gestation, coincident with the period of maximal fetal growth, has no major effect on adiposity but results in greater abundance of specific mitochondrial proteins, i.e. voltage-dependent anion channel and/or uncoupling protein 2. These adaptations may increase the predisposal of these offspring to adult obesity. Increasing maternal nutrition in late gestation, however, can result in proportionately less fetal adipose tissue deposition in conjunction with enhanced abundance of uncoupling protein 1.

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Shankar, Ramya, Arulmozhi Ramarajan, Susheela Rani, and V. Seshiah. "Anthropometric and Skin Fold Thickness Measurements of Newborns of Gestational Glucose Intolerant Mothers: Does it Indicate Disproportionate Fetal Growth?" Journal of Obstetrics and Gynecology of India 70, no. 6 (August 25, 2020): 471–78. http://dx.doi.org/10.1007/s13224-020-01340-6.

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Abstract Aim of the Study Studies have shown that gestational diabetes mellitus (GDM) causes disproportionate growth and increased adiposity in their newborns; however, the effect of gestational glucose intolerance (GGI), i.e., 2 h plasma glucose (PG) between 120 and 139 mg/dl in pregnancy on their newborns growth and adiposity is not well established. The objective of the present study is to evaluate the effect of GGI in pregnancy on anthropometry and adiposity of their newborns at birth in urban South Indian population. Materials and Methods An observational study was conducted on 119 urban South Indian pregnant women and their newborns. PG levels 2 h after ingestion of 75 g glucose load were determined between 24 and 28 weeks of gestation, and depending on their PG levels, these women were categorized into three different groups, (a) normal glucose tolerance (NGT)-2 h PG < 120 mg/dl, (b) GGI-2 h PG between 120 and 139 mg/dl and (c) GDM-2 h PG > or = 140 mg/dl. GDM mothers were treated with insulin and MNT advised. GGI mothers were advised MNT. These women were followed up till delivery. After delivery, their newborn’s anthropometry like weight, length, head circumference (HC), chest circumference (CC), mid-arm circumference, abdominal circumference, bisacromial diameter and subscapular and triceps skin fold thicknesses (SFT) was measured within 72 h of birth. Effect of GGI in pregnancy on newborn’s anthropometry and SFT was analyzed and studied in comparison with newborns of other two categories. Further, the newborns were stratified into four groups according to their birth weight and newborns of GGI category were compared with newborns of other two categories of same weight. Results The triceps and subscapular skin fold thicknesses which are direct measurements of adiposity were significantly higher in newborns of GGI mothers compared to newborns of GDM and NGT mothers. GGI category newborns showed increased adiposity even when they were compared with newborns of GDM and NGT category of same weight. Also measurements which are likely to increase due to increased adiposity like bisacromial diameter, abdominal circumference, mid-arm circumference were significantly higher in GGI category newborns. On the other hand, measurements which indicate skeletal growth like length, HC, CC were similar in all three category newborns. This confirmed disproportionate growth and increased adiposity in newborns of GGI mothers. It should be noted here that the GDM mothers were on MNT and treated with insulin, the dose of insulin was adjusted so as to mimick Fasting PG and Post Prandial PG levels of NGT mothers. Conclusion Gestational glucose intolerance during pregnancy does cause disproportionate growth (increased fat body mass but not skeletal mass) and increased adiposity in their newborns. This emphasizes the need for strict glycemic control (2 h of PG level after 75 grams glucose load to < 120 mg/dl and PPPG levels to < 120 mg/dl) during pregnancy. Larger multicentered studies are recommended to confirm this association.

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Almeida, V. R., V. S. Morita, S. Sgavioli, T. I. Vicentini, D. M. C. Castiblanco, and I. C. Boleli. "Incubation temperature manipulation during fetal development reduces adiposity of broiler hatchlings." Poultry Science 95, no. 2 (February 2016): 316–24. http://dx.doi.org/10.3382/ps/pev327.

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Wang, H., X. D. Yu, L. S. Huang, Q. Chen, F. X. Ouyang, X. Wang, and J. Zhang. "Fetal vitamin D concentration and growth, adiposity and neurodevelopment during infancy." European Journal of Clinical Nutrition 72, no. 10 (January 18, 2018): 1396–403. http://dx.doi.org/10.1038/s41430-017-0075-9.

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Chu, Anne H. Y., Mya T. Tint, Hsin F. Chang, Gerard Wong, Wen Lun Yuan, Dedreia Tull, Brunda Nijagal, et al. "High placental inositol content associated with suppressed pro-adipogenic effects of maternal glycaemia in offspring: the GUSTO cohort." International Journal of Obesity 45, no. 1 (May 20, 2020): 247–57. http://dx.doi.org/10.1038/s41366-020-0596-5.

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Abstract Background/Objectives Maternal glycaemia promotes fetal adiposity. Inositol, an insulin sensitizer, has been trialled for gestational diabetes prevention. The placenta has been implicated in how maternal hyperglycaemia generates fetal pathophysiology, but no studies have examined whether placental inositol biology is altered with maternal hyperglycaemia, nor whether such alterations impact fetal physiology. We aimed to investigate whether the effects of maternal glycaemia on offspring birthweight and adiposity at birth differed across placental inositol levels. Methods Using longitudinal data from the Growing Up in Singapore Towards healthy Outcomes cohort, maternal fasting glucose (FPG) and 2-hour plasma glucose (2hPG) were obtained in pregnant women by a 75-g oral glucose tolerance test around 26 weeks’ gestation. Relative placental inositol was quantified by liquid chromatography-mass spectrometry. Primary outcomes were birthweight (n = 884) and abdominal adipose tissue (AAT) volumes measured by neonatal MRI scanning in a subset (n = 262) of term singleton pregnancies. Multiple linear regression analyses were performed. Results Placental inositol was lower in those with higher 2hPG, no exposure to tobacco smoke antenatally, with vaginal delivery and shorter gestation. Positive associations of FPG with birthweight (adjusted β [95% CI] 164.8 g [109.1, 220.5]) and AAT (17.3 ml [11.9, 22.6] per mmol glucose) were observed, with significant interactions between inositol tertiles and FPG in relation to these outcomes (p < 0.05). Stratification by inositol tertiles showed that each mmol/L increase in FPG was associated with increased birthweight and AAT volume among cases within the lowest (birthweight = 174.2 g [81.2, 267.2], AAT = 21.0 ml [13.1, 28.8]) and middle inositol tertiles (birthweight = 202.0 g [103.8, 300.1], AAT = 19.7 ml [9.7, 29.7]). However, no significant association was found among cases within the highest tertile (birthweight = 81.0 g [−21.2, 183.2], AAT = 0.8 ml [−8.4, 10.0]). Conclusions High placental inositol may protect the fetus from the pro-adipogenic effects of maternal glycaemia. Studies are warranted to investigate whether prenatal inositol supplementation can increase placental inositol and reduce fetal adiposity.

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Marshall, Nicole, Kent Thornburg, and Jonathan Purnell. "Sex Related Impact of Maternal Adiposity on Neonatal Adiposity and Metabolic Status." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1033. http://dx.doi.org/10.1093/cdn/nzaa054_105.

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Abstract Objectives Women with obesity are at increased risk to have large for gestational age neonates. Our study aimed to understand the association between maternal adiposity and neonatal adiposity and metabolic markers. Methods This was a prospective cohort study of healthy women with singleton pregnancies enrolled at 12–16 or 37–38 weeks gestation. Maternal fat mass was determined by air displacement plethysmography. Infant fat mass was determined by skin fold thickness. Cord blood was collected at delivery. Linear regression was used to determine the association of maternal adiposity with infant birth weight, fat mass, and glucose, insulin, lipid, and adipokine levels. Results One hundred eighty five women were enrolled. Demographics (mean, min-max): maternal age 32.9 years (18.8–43.8), maternal pre-pregnancy BMI 27.2 kg/m,2 (17.5–54.0), gestational age at delivery 39.5 weeks (34–42), birthweight 3.46 kg (2.1–5.0). Newborn leptin levels were associated with maternal pre-pregnancy BMI (p-value 0.0070, r2 0.0468), maternal fat mass at 12 and 37 weeks, and maternal %body fat at 12 and 37 weeks. There were no others associations among maternal adiposity and infant adiposity or metabolic markers. When analyzed by fetal sex, female infant birthweight was associated with maternal pre-pregnancy BMI (p-value 0.025, r2 0.055), female fat mass was associated with pre-pregnancy BMI and maternal fat mass at 37 weeks (p-value 0.024, r2 0.069), and female %body fat was associated with maternal fat mass at 37 weeks (p-value 0.0239, r2 0.069). Female infant HDL was lower at birth with increasing maternal fat mass at 12 weeks gestation (p-value 0.0405, r2 0.121). Female infant leptin levels were increased with maternal adiposity including pre-pregnancy BMI, maternal fat mass at 37 weeks, maternal %body fat, and gestational weight gain. Female infant adiponectin levels were lower with increasing maternal pre-pregnancy BMI (p-value 0.0468, r2 0.0538). There were no associations between maternal adiposity and male infant adiposity or metabolic markers. Conclusions Maternal adiposity was associated with increased neonatal leptin levels, but not neonatal adiposity or metabolic markers. Female, but not male, infants had higher birthweight, fat mass, %body fat, and leptin levels and lower HDL and adiponectin levels with increasing maternal adiposity. Funding Sources NICHD.

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De Blasio, Miles J., Kathryn L. Gatford, I. Caroline McMillen, Jeffrey S. Robinson, and Julie A. Owens. "Placental Restriction of Fetal Growth Increases Insulin Action, Growth, and Adiposity in the Young Lamb." Endocrinology 148, no. 3 (March 1, 2007): 1350–58. http://dx.doi.org/10.1210/en.2006-0653.

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Most children who are short or light at birth due to intrauterine growth restriction (IUGR) exhibit accelerated growth in infancy, termed “catch-up” growth, which together with IUGR, predicts increased risk of type 2 diabetes and obesity later in life. Placental restriction (PR) in sheep reduces size at birth, and also causes catch-up growth and increased adiposity at 6 wk of age. The physiological mechanisms responsible for catch-up growth after IUGR and its links to these adverse sequelae are unknown. Because insulin is a major anabolic hormone of infancy and its actions are commonly perturbed in these related disorders, we hypothesized that restriction of fetal growth would alter insulin secretion and sensitivity in the juvenile sheep at 1 month, which would be related to their altered growth and adiposity. We show that PR impairs glucose-stimulated insulin production, but not fasting insulin abundance or production in the young sheep. However, PR increases insulin sensitivity of circulating free fatty acids (FFAs), and insulin disposition indices for glucose and FFAs. Catch-up growth is predicted by the insulin disposition indices for amino acids and FFAs, and adiposity by that for FFAs. This suggests that catch-up growth and early-onset visceral obesity after IUGR may have a common underlying cause, that of increased insulin action due primarily to enhanced insulin sensitivity, which could account in part for their links to adverse metabolic and related outcomes in later life.

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Gagné-Ouellet, Valérie, Edith Breton, Kathrine Thibeault, Carol-Ann Fortin, Véronique Desgagné, Élise Girard Tremblay, Andres Cardenas, et al. "Placental Epigenome-Wide Association Study Identified Loci Associated with Childhood Adiposity at 3 Years of Age." International Journal of Molecular Sciences 21, no. 19 (September 29, 2020): 7201. http://dx.doi.org/10.3390/ijms21197201.

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The aim of this study was to identify placental DNA methylation (DNAm) variations associated with adiposity at 3 years of age. We quantified placental DNAm using the Infinium MethylationEPIC BeadChips. We assessed associations between DNAm at single-CpGs and skinfold thickness using robust linear regression models adjusted for gestational age, child’s sex, age at follow-up and cellular heterogeneity. We sought replication of DNAm association with child adiposity in an independent cohort. We quantified placental mRNA levels for annotated gene using qRT-PCR and tested for correlation with DNAm. Lower DNAm at cg22593959 and cg22436429 was associated with higher adiposity (β = −1.18, q = 0.002 and β = −0.82, q = 0.04). The cg22593959 is located in an intergenic region (chr7q31.3), whereas cg22436429 is within the TFAP2E gene (1p34.3). DNAm at cg22593959 and cg22436429 was correlated with mRNA levels at FAM3C (rs = −0.279, p = 0.005) and TFAP2E (rs = 0.216, p = 0.03). In an independent cohort, the association between placental DNAm at cg22593959 and childhood adiposity was of similar strength and direction (β = −3.8 ± 4.1, p = 0.36), yet non-significant. Four genomic regions were also associated with skinfold thickness within FMN1, MAGI2, SKAP2 and BMPR1B genes. We identified placental epigenetic variations associated with adiposity at 3 years of age suggesting that childhood fat accretion patterns might be established during fetal life.

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Pilgaard, Kasper, Thomas Hammershaimb Mosbech, Louise Grunnet, Hans Eiberg, Gerrit Van Hall, Eva Fallentin, Torben Larsen, Rasmus Larsen, Pernille Poulsen, and Allan Vaag. "Differential Nongenetic Impact of Birth Weight Versus Third-Trimester Growth Velocity on Glucose Metabolism and Magnetic Resonance Imaging Abdominal Obesity in Young Healthy Twins." Journal of Clinical Endocrinology & Metabolism 96, no. 9 (September 1, 2011): 2835–43. http://dx.doi.org/10.1210/jc.2011-0577.

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Abstract Context: Low birth weight is associated with type 2 diabetes, which to some extent may be mediated via abdominal adiposity and insulin resistance. Fetal growth velocity is high during the third trimester, constituting a potential critical window for organ programming. Intra-pair differences among monozygotic twins are instrumental in determining nongenetic associations between early environment and adult metabolic phenotype. Objective: Our objective was to investigate the relationship between size at birth and third-trimester growth velocity on adult body composition and glucose metabolism using intra-pair differences in young healthy twins. Methods: Fifty-eight healthy twins (42 monozygotic/16 dizygotic) aged 18–24 yr participated. Insulin sensitivity was assessed using hyperinsulinemic-euglycemic clamps. Whole-body fat was assessed by dual-energy x-ray absorptiometry scan, whereas abdominal visceral and sc fat (L1–L4) were assessed by magnetic resonance imaging. Third-trimester growth velocity was determined by repeated ultrasound examinations. Results: Size at birth was nongenetically inversely associated with adult visceral and sc fat accumulation but unrelated to adult insulin action. In contrast, fetal growth velocity during third trimester was not associated with adult visceral or sc fat accumulation. Interestingly, third-trimester growth was associated with insulin action in a paradoxical inverse manner. Conclusions: Abdominal adiposity including accumulation of both sc and visceral fat may constitute primary nongenetic factors associated with low birth weight and reduced fetal growth before the third trimester. Reduced fetal growth during vs. before the third trimester may define distinct adult trajectories of metabolic and anthropometric characteristics influencing risk of developing type 2 diabetes.

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Dimas, Angelos, Anastasia Politi, George Papaioannou, Thomas M. Barber, Martin O. Weickert, Dimitris K. Grammatopoulos, Sudhesh Kumar, Sophia Kalantaridou, and Georgios Valsamakis. "The Gestational Effects of Maternal Appetite Axis Molecules on Fetal Growth, Metabolism and Long-Term Metabolic Health: A Systematic Review." International Journal of Molecular Sciences 23, no. 2 (January 9, 2022): 695. http://dx.doi.org/10.3390/ijms23020695.

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Increased maternal food intake is considered a normal pregnancy adjustment. However, the overavailability of nutrients may lead to dysregulated fetal development and increased adiposity, with long-lasting effects on offspring in later life. Several gut-hormone molecules regulate maternal appetite, with both their orexigenic and anorectic effects being in a state of sensitive equilibrium. The aim of this manuscript is to systematically review literature on the effects of maternal gut-hormone molecules on fetal growth and metabolism, birth weight and the later metabolic health of offspring. Maternal serum ghrelin, leptin, IGF-1 and GLP-1 appear to influence fetal growth; however, a lack of consistent and strong correlations of maternal appetite axis hormones with birth weight and the concomitant correlation with fetal and birth waist circumference may suggest that these molecules primarily mediate fetal energy deposition mechanisms, preparing the fetus for survival after birth. Dysregulated intrauterine environments seem to have detrimental, sex-dependent effects on fetal energy stores, affecting not only fetal growth, fat mass deposition and birth weight, but also future metabolic and endocrine wellbeing of offspring.

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Ikenoue, S., F. Waffarn, K. Sumiyoshi, M. Ohashi, C. Ikenoue, C. Buss, D. L. Gillen, H. N. Simhan, S. Entringer, and P. D. Wadhwa. "Association of ultrasound-based measures of fetal body composition with newborn adiposity." Pediatric Obesity 12 (November 29, 2016): 86–93. http://dx.doi.org/10.1111/ijpo.12198.

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Blumfield, Michelle L., Alexis J. Hure, Lesley K. MacDonald-Wicks, Roger Smith, Stephen J. Simpson, Warwick B. Giles, David Raubenheimer, and Clare E. Collins. "Dietary balance during pregnancy is associated with fetal adiposity and fat distribution." American Journal of Clinical Nutrition 96, no. 5 (October 3, 2012): 1032–41. http://dx.doi.org/10.3945/ajcn.111.033241.

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Lewis, R. M., H. Demmelmair, R. Gaillard, K. M. Godfrey, S. Hauguel-de Mouzon, B. Huppertz, E. Larque, R. Saffery, M. E. Symonds, and G. Desoye. "The Placental Exposome: Placental Determinants of Fetal Adiposity and Postnatal Body Composition." Annals of Nutrition and Metabolism 63, no. 3 (2013): 208–15. http://dx.doi.org/10.1159/000355222.

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Catalano, Patrick M., Alicia Thomas, Larraine Huston-Presley, and Saeid B. Amini. "Increased fetal adiposity: A very sensitive marker of abnormal in utero development." American Journal of Obstetrics and Gynecology 189, no. 6 (December 2003): 1698–704. http://dx.doi.org/10.1016/s0002-9378(03)00828-7.

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Walsh, JM, M. Wallace, L. Brennan, and FM McAuliffe. "Early pregnancy maternal urinary metabolomic profile to predict fetal adiposity and macrosomia." Archives of Disease in Childhood - Fetal and Neonatal Edition 97, Suppl 1 (April 2012): A31.1—A31. http://dx.doi.org/10.1136/fetalneonatal-2012-301809.99.

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Hure, A. J., R. Smith, W. Giles, D. Somerset, and C. E. Collins. "P2-114 Fetal fatness is not associated with maternal adiposity in pregnancy." Early Human Development 83 (September 2007): S161. http://dx.doi.org/10.1016/s0378-3782(07)70447-4.

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Ibáñez, Lourdes, Abel López-Bermejo, and Francis de Zegher. "Pubertal adiposity after fetal growth restraint: toward a calorie restriction mimetic approach." Metabolism 57, no. 5 (May 2008): 672–75. http://dx.doi.org/10.1016/j.metabol.2008.01.002.

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