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Journal articles on the topic 'Intrauterine programming'

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Published: 10 December 2022

Last updated: 28 January 2023

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1

Lister, Rolanda. "Intrauterine Programming of Diabetes Induced Cardiac Embryopathy." Diabetes & Obesity International Journal 4, no. 3 (2019): 1–14. http://dx.doi.org/10.23880/doij-16000202.

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Background: Maternal hyperglycemia is a well-recognized risk factor for fetal congenital heart disease. However, the underlying cellular and molecular mechanisms are not well characterized. We hypothesize that maternal hyperglycemia leading to congenital heart are linked to abnormal DNA methylation and mRNA expression at cardiac specific loci. Methods: Hyperglycemia was induced in normal 8-week old CD-1 female mice with a one-time intraperitoneal injection of 150 mg/kg of streptozotocin (STZ) 2 weeks prior to mating. Histological analysis of fetal cardiac morphology was evaluated for malformations on embryonic day (E) 16.5 of control pups and pups exposed to maternal hyperglycemia. We used a massively-parallel sequencing-based methylation sensitive restriction based assay to examine genome-wide cytosine methylation levels at >1.65 million loci in neonatal hearts on post-natal (P) day 0. Functional validation was performed with real time quantitative polymerase chain reaction (RT-qPCR). Results: Cardiac structural defects occurred in 28% of the pups (n=12/45) of hyperglycemic dams versus 7% (n=4/61) of controls. Notable phenotypes were hypoplastic left or right ventricle, double outlet right ventricle, ventricular septal defect, and left ventricular outflow tract obstruction. A 10-fold increase in DNA methylation of gene promoter regions was seen in many cardiac important genes in the experimental versus control P0 neonates and have corresponding decreases in gene expression in 21/32 genes functionally validated. Conclusion: Maternal hyperglycemia alters DNA methylation and mRNA expression of some cardiac genes during heart development. Quantitative, genome-wide assessment of cytosine methylation can be used as a discovery platform to gain insight into the mechanisms of hyperglycemia-induced cardiac anomalies.

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2

Fernandez‐Capetillo, Oscar. "Intrauterine programming of ageing." EMBO reports 11, no. 1 (December 11, 2009): 32–36. http://dx.doi.org/10.1038/embor.2009.262.

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3

Fowden, A. L., and A. J. Forhead. "Endocrine mechanisms of intrauterine programming." Reproduction 127, no. 5 (May 2004): 515–26. http://dx.doi.org/10.1530/rep.1.00033.

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Epidemiological findings and experimental studies in animals have shown that individual tissues and whole organ systems can be programmedin uteroduring critical periods of development with adverse consequences for their function in later life. Detailed morphometric analyses of the data have shown that certain patterns of intrauterine growth, particularly growth retardation, can be related to specific postnatal outcomes. Since hormones regulate fetal growth and the development of individual fetal tissues, they have a central role in intrauterine programming. Hormones such as insulin, insulin-like growth factors, thyroxine and the glucocorticoids act as nutritional and maturational signals and adapt fetal development to prevailing intrauterine conditions, thereby maximizing the chances of survival bothin uteroand at birth. However, these adaptations may have long-term sequelae. Of the hormones known to control fetal development, it is the glucocorticoids that are most likely to cause tissue programmingin utero. They are growth inhibitory and affect the development of all the tissues and organ systems most at risk of postnatal pathophysiology when fetal growth is impaired. Their concentrationsin uteroare also elevated by all the nutritional and other challenges known to have programming effects. Glucocorticoids act at cellular and molecular levels to alter cell function by changing the expression of receptors, enzymes, ion channels and transporters. They also alter various growth factors, cytoarchitectural proteins, binding proteins and components of the intracellular signalling pathways. Glucocorticoids act, directly, on genes and, indirectly, through changes in the bioavailability of other hormones. These glucocorticoid-induced endocrine changes may be transient or persist into postnatal life with consequences for tissue growth and development both before and after birth. In the long term, prenatal glucocorticoid exposure can permanently reset endocrine systems, such as the somatotrophic and hypothalamic–pituitary–adrenal axes, which, in turn, may contribute to the pathogenesis of adult disease. Endocrine changes may, therefore, be both the cause and the consequence of intrauterine programming.

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4

Ige, S. F., R. E. Akhigbe, and O. O. Akinsemola. "Intrauterine Programming and Postnatal Hypertension." Research Journal of Obstetrics and Gynecology 4, no. 1 (January 1, 2011): 1–27. http://dx.doi.org/10.3923/rjog.2011.1.27.

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5

Barker, David J. P. "Intrauterine programming of adult disease." Molecular Medicine Today 1, no. 9 (December 1995): 418–23. http://dx.doi.org/10.1016/s1357-4310(95)90793-9.

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6

Fowden, A. L., O. A. Valenzuela, O. R. Vaughan, J. K. Jellyman, and A. J. Forhead. "Glucocorticoid programming of intrauterine development." Domestic Animal Endocrinology 56 (July 2016): S121—S132. http://dx.doi.org/10.1016/j.domaniend.2016.02.014.

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7

Fowden, A. L., A. J. Forhead, P. M. Coan, and G. J. Burton. "The Placenta and Intrauterine Programming." Journal of Neuroendocrinology 20, no. 4 (April 2008): 439–50. http://dx.doi.org/10.1111/j.1365-2826.2008.01663.x.

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8

Remacle, C., O. Dumortier, V. Bol, K. Goosse, P. Romanus, N. Theys, T. Bouckenooghe, and B. Reusens. "Intrauterine programming of the endocrine pancreas." Diabetes, Obesity and Metabolism 9, s2 (November 2007): 196–209. http://dx.doi.org/10.1111/j.1463-1326.2007.00790.x.

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9

Gale, C. R. "Intrauterine Programming of Adult Body Composition." Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 1, 2001): 267–72. http://dx.doi.org/10.1210/jc.86.1.267.

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10

Gale, Catharine R., Christopher N. Martyn, Samantha Kellingray, Richard Eastell, and Cyrus Cooper. "Intrauterine Programming of Adult Body Composition1." Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 2001): 267–72. http://dx.doi.org/10.1210/jcem.86.1.7155.

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11

Langley-Evans, Simon C. "Intrauterine programming of hypertension by glucocorticoids." Life Sciences 60, no. 15 (March 1997): 1213–21. http://dx.doi.org/10.1016/s0024-3205(96)00611-x.

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12

Arany, Edith. "Intrauterine programming of beta cell defects." Placenta 36, no. 4 (April 2015): 474–75. http://dx.doi.org/10.1016/j.placenta.2015.01.399.

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13

Tomar, Ashutosh Singh, Divya Sri Priyanka Tallapragada, Suraj Singh Nongmaithem, Smeeta Shrestha, Chittaranjan S. Yajnik, and Giriraj Ratan Chandak. "Intrauterine Programming of Diabetes and Adiposity." Current Obesity Reports 4, no. 4 (September 8, 2015): 418–28. http://dx.doi.org/10.1007/s13679-015-0175-6.

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14

Gardiner, H. M. "Intrauterine programming of the cardiovascular system." Ultrasound in Obstetrics and Gynecology 32, no. 4 (September 2008): 481–84. http://dx.doi.org/10.1002/uog.6155.

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15

Fowden, Abigail L., Dino A. Giussani, and Alison J. Forhead. "Intrauterine Programming of Physiological Systems: Causes and Consequences." Physiology 21, no. 1 (February 2006): 29–37. http://dx.doi.org/10.1152/physiol.00050.2005.

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The intrauterine conditions in which the mammalian fetus develops have an important role in regulating the function of its physiological systems later in life. Changes in the intrauterine availability of nutrients, oxygen, and hormones program tissue development and lead to abnormalities in adult cardiovascular and metabolic function in several species. The timing, duration, severity, and type of insult during development determines the specific physiological outcome. Intrauterine programming of physiological systems occurs at the gene, cell, tissue, organ, and system levels and causes permanent structural and functional changes, which can lead to overt disease, particularly with increasing age.

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16

Zhuk, S. I., and O. D. Shchurevska. "Fetal stress-programming." HEALTH OF WOMAN, no. 1(117) (February 28, 2017): 116–19. http://dx.doi.org/10.15574/hw.2017.117.116.

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Numerous recent studies demonstrate the important role of the prenatal period in the formation of obesity, hypertension and carbohydrate tolerance impairment in adulthood. The article presents the literature and our own data on the hormonal and epigenetic mechanisms of this diseases. Antenatal and postnatal markers of intrauterine programming were described. Key words: stress, pregnancy, fetal programming, miRNA, metabolic syndrome.

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17

Xu, Dan, Jing Bai, Li Zhang, Lang Shen, Linlong Wang, Zhongfen Liu, Liping Xia, and Hui Wang. "Prenatal nicotine exposure-induced intrauterine programming alteration increases the susceptibility of high-fat diet-induced non-alcoholic simple fatty liver in female adult offspring rats." Toxicology Research 4, no. 1 (2015): 112–20. http://dx.doi.org/10.1039/c4tx00092g.

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18

Dzgoeva, Fatima Khadzhimuratovna. "Intrauterine nutrition: fetal programming of metabolic syndrome." Obesity and metabolism 12, no. 3 (August 10, 2015): 10–17. http://dx.doi.org/10.14341/omet2015310-17.

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Research investigating the early programming includes studies addressing the role of intrauterine nutrient availability, which is determined by maternal nutrition. This review will explore the epidemiological evidence for programming of metabolic disease and it will also discuss evidence for the proposed molecular mechanisms and the potential for intervention.

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19

Langley-Evans, Simon, and Alan Jackson. "Intrauterine Programming of Hypertension: Nutrient-Hormone Interactions." Nutrition Reviews 54, no. 6 (April 27, 2009): 163–69. http://dx.doi.org/10.1111/j.1753-4887.1996.tb03923.x.

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20

Fowden, Abigail L., Dino A. Giussani, and Alison J. Forhead. "Endocrine and metabolic programming during intrauterine development." Early Human Development 81, no. 9 (September 2005): 723–34. http://dx.doi.org/10.1016/j.earlhumdev.2005.06.007.

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21

Nagaeva, E. V., and T. Iu Shiriaeva. ""Intrauterine programming" of hormonal and metabolic processes and intrauterine growth retardation syndrome." Problems of Endocrinology 56, no. 6 (December 15, 2010): 32–40. http://dx.doi.org/10.14341/probl201056632-40.

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According to the "intrauterine programming" hypothesis, the fetus responses to nutritional deficiency by adaptation in the form of long-standing changes of metabolism that eventually create predisposition to cardiovascular, metabolic, and endocrine diseases. Up to now, a wealth of catamnestic data have been gathered indicating that individuals having the history of growth retardation in the prenatal period are likely to develop a variety of hormonal and metabolic disorders when they reach their mature age. Specifically, there is the close relationship between the intrauterine growth retardation syndrome and elevated arterial pressure, impaired glucose tolerance, and metabolic syndrome. The present review summarizes the results of epidemiological and experimental studies that confirm the above hypothesis.

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22

Lu, Juan, Yinxian Wen, Li Zhang, Chong Zhang, Weihua Zhong, Lu Zhang, Ying Yu, Liaobin Chen, Dan Xu, and Hui Wang. "Prenatal ethanol exposure induces an intrauterine programming of enhanced sensitivity of the hypothalamic–pituitary–adrenal axis in female offspring rats fed with post-weaning high-fat diet." Toxicology Research 4, no. 5 (2015): 1238–49. http://dx.doi.org/10.1039/c5tx00012b.

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23

Sandakova, E. A., and I. G. Zhukovskaya. "Fetal programming." Medical alphabet 2, no. 14 (December 2, 2019): 17–20. http://dx.doi.org/10.33667/2078-5631-2019-2-14(389)-17-20.

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The concept of fetal programming implies the influence of factors of the external and internal environment in the intrauterine period on the epigenetic regulation of the genome, which leads to phenotypic changes in the fetus, as well as to postnatal diseases of man, manifesting throughout life. It is possible to improve the state of health, quality and life expectancy of offspring, as well as subsequent generations, due to the pregravidar preparation of both parents, the modification of their lifestyle, the abandonment of bad habits, the rationalization of nutrition, and the donation of vitamin and mineral complexes.

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24

Eberle, Claudia, and Christoph Ament. "Diabetic and Metabolic Programming: Mechanisms Altering the Intrauterine Milieu." ISRN Pediatrics 2012 (November 20, 2012): 1–11. http://dx.doi.org/10.5402/2012/975685.

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A wealth of epidemiological, clinical, and experimental studies have been linked to poor intrauterine conditions as well as metabolic and associated cardiovascular changes postnatal. These are novel perspectives connecting the altered intrauterine milieu to a rising number of metabolic diseases, such as diabetes, obesity, and hypercholesterolemia as well as the Metabolic Syndrome (Met S). Moreover, metabolic associated atherosclerotic diseases are connected to perigestational maternal health. The “Thrifty Phenotype Hypothesis” introduced cross-generational links between poor conditions during gestation and metabolic as well as cardiovascular alterations postnatal. Still, mechanisms altering the intrauterine milieu causing metabolic and associated atherosclerotic diseases are currently poorly understood. This paper will give novel insights in fundamental concepts connected to specific molecular mechanisms “programming” diabetes and associated metabolic as well as cardiovascular diseases.

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25

Kovtun, O. P., and P. B. Tsyvian. "Pre-eclampsia in a mother and programming of the child’s cardiovascular health." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, no. 4 (September 15, 2019): 19–25. http://dx.doi.org/10.21508/1027-4065-2019-64-4-19-25.

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The authors present a review of the literature devoted to the problem of programming the formation of the cardiovascular system structure and function in children born from mothers with preeclampsia. These children are at high risk of developing cardiovascular diseases. Pre-eclampsia is caused by the endothelium dysfunction, deregulation of the immune and inflammatory factors during pregnancy. Experimental studies identify these factors as key epigenetic factors programming the condition of the cardiovascular system of the offspring. The modern concept of intrauterine programming, describing this phenomenon, focuses on three main areas of research: experimental models simulating the intrauterine environment with preeclampsia; research of the pathological phenotype formation under the influence of these factors; epigenetic studies of the influence of preeclampsia on the cardiovascular system functioning. The article discusses the perspectives of epigenetic programming prevention.

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26

Barker, DJP. "Intrauterine programming of coronary heart disease and stroke." Acta Paediatrica 86, S423 (November 1997): 178–82. http://dx.doi.org/10.1111/j.1651-2227.1997.tb18408.x.

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27

Jawerbaum, Alicia. "Novel model of GDM induced by intrauterine programming." Placenta 57 (September 2017): 242. http://dx.doi.org/10.1016/j.placenta.2017.07.071.

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28

Lister, Rolanda, Bin Zhou, Alyssa Chamberlain, and Francine Einstein. "61: Intrauterine programming of diabetes induced cardiac embryopathy." American Journal of Obstetrics and Gynecology 208, no. 1 (January 2013): S36. http://dx.doi.org/10.1016/j.ajog.2012.10.235.

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29

Fernandez-Twinn, Denise S., Line Hjort, Boris Novakovic, Susan E. Ozanne, and Richard Saffery. "Intrauterine programming of obesity and type 2 diabetes." Diabetologia 62, no. 10 (August 27, 2019): 1789–801. http://dx.doi.org/10.1007/s00125-019-4951-9.

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30

Stanner, Sara A., and John S. Yudkin. "Fetal Programming and the Leningrad Siege Study." Twin Research 4, no. 5 (October 1, 2001): 287–92. http://dx.doi.org/10.1375/twin.4.5.287.

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AbstractThe Leningrad Siege Study investigated the relationship between decreased maternal food intake and risk factors for coronary heart disease in adult life. The study screened 169 subjects exposed to intrauterine starvation during the Siege of Leningrad (now St Petersburg) 1941–4, 192 subjects born in Leningrad before the siege and 188 subjects born concurrently with these two groups but outside the area of the siege. No difference was found between the subjects exposed to starvation in utero and during infancy in glucose tolerance [in utero: 5.2 mmol/l (95% confidence interval 5.1 to 5.3; infancy: 5.3 (5.1 to 5.5), p = 0.94], insulin concentration, blood pressure, lipid concentration or coagulation factors. The intrauterine exposed group had evidence of endothelial dysfunction by higher concentrations of von Willebrand factor and a stronger interaction between adult obesity and blood pressure. Non-systematic differences in subscapular to triceps skinfold ratio, diastolic blood pressure and clotting factors were demonstrated compared to the non-exposed groups. In conclusion, this study did not find an association between intrauterine starvation and glucose intolerance, dyslipidaemia, hypertension or cardiovascular disease in adult life. These findings differ from studies of subjects exposed to maternal starvation during the Dutch Hunger Winter. However, the dissimilar effects of exposure to the two famines may contribute to our understanding of the mechanisms of the ‘thrifty phenotype’ and support the importance of catch-up growth during early childhood, a situation that occurred in the Netherlands but not in Leningrad.

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31

Tong, Yajie, Shuqing Zhang, Suzette Riddle, Lubo Zhang, Rui Song, and Dongmei Yue. "Intrauterine Hypoxia and Epigenetic Programming in Lung Development and Disease." Biomedicines 9, no. 8 (August 2, 2021): 944. http://dx.doi.org/10.3390/biomedicines9080944.

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Clinically, intrauterine hypoxia is the foremost cause of perinatal morbidity and developmental plasticity in the fetus and newborn infant. Under hypoxia, deviations occur in the lung cell epigenome. Epigenetic mechanisms (e.g., DNA methylation, histone modification, and miRNA expression) control phenotypic programming and are associated with physiological responses and the risk of developmental disorders, such as bronchopulmonary dysplasia. This developmental disorder is the most frequent chronic pulmonary complication in preterm labor. The pathogenesis of this disease involves many factors, including aberrant oxygen conditions and mechanical ventilation-mediated lung injury, infection/inflammation, and epigenetic/genetic risk factors. This review is focused on various aspects related to intrauterine hypoxia and epigenetic programming in lung development and disease, summarizes our current knowledge of hypoxia-induced epigenetic programming and discusses potential therapeutic interventions for lung disease.

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32

Entringer, Sonja, Claudia Buss, James M. Swanson, Dan M. Cooper, Deborah A. Wing, Feizal Waffarn, and Pathik D. Wadhwa. "Fetal Programming of Body Composition, Obesity, and Metabolic Function: The Role of Intrauterine Stress and Stress Biology." Journal of Nutrition and Metabolism 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/632548.

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Epidemiological, clinical, physiological, cellular, and molecular evidence suggests that the origins of obesity and metabolic dysfunction can be traced back to intrauterine life and supports an important role for maternal nutrition prior to and during gestation in fetal programming. The elucidation of underlying mechanisms is an area of interest and intense investigation. In this perspectives paper we propose that in addition to maternal nutrition-related processes it may be important to concurrently consider the potential role of intrauterine stress and stress biology. We frame our arguments in the larger context of an evolutionary-developmental perspective that supports roles for both nutrition and stress as key environmental conditions driving natural selection and developmental plasticity. We suggest that intrauterine stress exposure may interact with the nutritional milieu, and that stress biology may represent an underlying mechanism mediating the effects of diverse intrauterine perturbations, including but not limited to maternal nutritional insults (undernutrition and overnutrition), on brain and peripheral targets of programming of body composition, energy balance homeostasis, and metabolic function. We discuss putative maternal-placental-fetal endocrine and immune/inflammatory candidate mechanisms that may underlie the long-term effects of intrauterine stress. We conclude with a commentary of the implications for future research and clinical practice.

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33

GATFORD, KATHRYN L., and REBECCA A. SIMMONS. "Prenatal Programming of Insulin Secretion in Intrauterine Growth Restriction." Clinical Obstetrics and Gynecology 56, no. 3 (September 2013): 520–28. http://dx.doi.org/10.1097/grf.0b013e31829e5b29.

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34

Langley-Evans, Simon C., David S. Gardner, and Simon J. M. Welham. "Intrauterine Programming of Cardiovascular Disease by Maternal Nutritional Status." Nutrition 14, no. 1 (January 1998): 39–47. http://dx.doi.org/10.1016/s0899-9007(97)00391-2.

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35

Langley-Evans, Simon C. "Intrauterine programming of hypertension in the rat: Nutrient interactions." Comparative Biochemistry and Physiology Part A: Physiology 114, no. 4 (August 1996): 327–33. http://dx.doi.org/10.1016/0300-9629(96)00018-7.

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36

Riesche, Laren, Suzette D. Tardif, Corinna N. Ross, Victoria A. deMartelly, Toni Ziegler, and Julienne N. Rutherford. "The common marmoset monkey: avenues for exploring the prenatal, placental, and postnatal mechanisms in developmental programming of pediatric obesity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 5 (May 1, 2018): R684—R692. http://dx.doi.org/10.1152/ajpregu.00164.2017.

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Animal models have been critical in building evidence that the prenatal experience and intrauterine environment are capable of exerting profound and permanent effects on metabolic health through developmental programming of obesity. However, despite physiological and evolutionary similarities, nonhuman primate models are relatively rare. The common marmoset monkey ( Callithrix jacchus) is a New World monkey that has been used as a biomedical model for well more than 50 years and has recently been framed as an appropriate model for exploring early-life impacts on later health and disease. The spontaneous, multifactorial, and early-life development of obesity in the common marmoset make it a valuable research model for advancing our knowledge about the role of the prenatal and placental mechanisms involved in developmental programming of obesity. This paper provides a brief overview of obesity in the common marmoset, followed by a discussion of marmoset reproduction and placental characteristics. We then discuss the occurrence and utility of variable intrauterine environments in developmental programming in marmosets. Evidence of developmental programming of obesity will be given, and finally, we put forward future directions and innovations for including the placenta in developmental programming of obesity in the common marmoset.

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37

Thompson, Loren P., Hong Song, and Brian M. Polster. "Fetal Programming and Sexual Dimorphism of Mitochondrial Protein Expression and Activity of Hearts of Prenatally Hypoxic Guinea Pig Offspring." Oxidative Medicine and Cellular Longevity 2019 (June 2, 2019): 1–11. http://dx.doi.org/10.1155/2019/7210249.

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Chronic intrauterine hypoxia is a programming stimulus of cardiovascular dysfunction. While the fetal heart adapts to the reduced oxygenation, the offspring heart becomes vulnerable to subsequent metabolic challenges as an adult. Cardiac mitochondria are key organelles responsible for an efficient energy supply but are subject to damage under hypoxic conditions. We propose that intrauterine hypoxia alters mitochondrial function as an underlying programming mechanism of contractile dysfunction in the offspring. Indices of mitochondrial function such as mitochondrial DNA content, Complex (C) I-V expression, and CI/CIV enzyme activity were measured in hearts of male and female offspring at 90 days old exposed to prenatal hypoxia (10.5% O2) for 14 d prior to term (65 d). Both left ventricular tissue and cardiomyocytes exhibited decreased mitochondrial DNA content, expression of CIV, and CI/CIV activity in male hearts. In female cardiomyocytes, hypoxia had no effect on protein expression of CI-CV nor on CI/CIV activity. This study suggests that chronic intrauterine hypoxia alters the intrinsic properties of select respiratory complexes as a programming mechanism of cardiac dysfunction in the offspring. Sex differences in mitochondrial function may underlie the increased vulnerability of age-matched males compared to females in cardiovascular disease and heart failure.

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38

Minabe, Shiori, Kinuyo Iwata, Youki Watanabe, and Hitoshi Ozawa. "ODP330 Long-term Effects of Prenatal Undernutrition on Hypothalamic KNDy Gene Expression in Female Rats." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A500. http://dx.doi.org/10.1210/jendso/bvac150.1039.

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Abstract Accumulating evidence suggested that the nutritional environment during development periods induces metabolic programming, leading to metabolic disorders and detrimental influences on human reproductive health. The purpose of this study was to determine whether intrauterine malnutrition has a long-term adverse effect on a reproductive center, kisspeptin-neurokinin B-dynorphin A (KNDy) neurons in the hypothalamic arcuate nucleus (ARC) of the female offspring. In female offspring from 50% undernutrition (UN) dams, first virginal estrus tended to be advanced, and hypothalamic neurokinin B gene (Tac3) expression was increased in adolescents. Conversely, the UN caused the significant suppression of ARC kisspeptin (Kiss1) and Tac3 gene expression after 29 weeks of age. These results suggested that intrauterine undernutrition stress caused developmental programming in KNDy neurons, which changed in their gene expression depending on life stages. Furthermore, our data showed obesogenic effects of prenatal undernutrition in the female rats; UN offspring showed low birth weight, rapid catch-up growth at four weeks of age, visceral fat accumulation, and an increase in calorie intake and plasma triglyceride levels at adulthood. The current study demonstrated that intrauterine undernutrition affected hypothalamic developmental programming in female rats, which induced long-term effects on hypothalamic KNDy gene expression and could influence metabolism and reproductive function later in life. Presentation: No date and time listed

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39

Ayres, Caroline, Marilyn Agranonik, André Krumel Portella, Françoise Filion, Celeste C. Johnston, and Patrícia Pelufo Silveira. "Intrauterine Growth Restriction and the Fetal Programming of the Hedonic Response to Sweet Taste in Newborn Infants." International Journal of Pediatrics 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/657379.

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Intrauterine growth restriction is associated with increased risk for adult metabolic syndrome and cardiovascular disease, which seems to be related to altered food preferences in these individuals later in life. In this study, we sought to understand whether intrauterine growth leads to fetal programming of the hedonic responses to sweet. Sixteen 1-day-old preterm infants received 24% sucrose solution or water and the taste reactivity was filmed and analyzed. Spearman correlation demonstrated a positive correlation between fetal growth and the hedonic response to the sweet solution in the first 15 seconds after the offer (r=0.864,P=0.001), without correlation when the solution given is water (r=0.314,P=0.455). In fact, the more intense the intrauterine growth restriction, the lower the frequency of the hedonic response observed. IUGR is strongly correlated with the hedonic response to a sweet solution in the first day of life in preterm infants. This is the first evidence in humans to demonstrate that the hedonic response to sweet taste is programmed very early during the fetal life by the degree of intrauterine growth. The altered hedonic response at birth and subsequent differential food preference may contribute to the increased risk of obesity and related disorders in adulthood in intrauterine growth-restricted individuals.

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40

Thompson, Loren P., and Yazan Al-Hasan. "Impact of Oxidative Stress in Fetal Programming." Journal of Pregnancy 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/582748.

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Intrauterine stress induces increased risk of adult disease through fetal programming mechanisms. Oxidative stress can be generated by several conditions, such as, prenatal hypoxia, maternal under- and overnutrition, and excessive glucocorticoid exposure. The role of oxidant molecules as signaling factors in fetal programming via epigenetic mechanisms is discussed. By linking oxidative stress with dysregulation of specific target genes, we may be able to develop therapeutic strategies that protect against organ dysfunction in the programmed offspring.

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41

Chong, Euming, and Ihor V. Yosypiv. "Developmental Programming of Hypertension and Kidney Disease." International Journal of Nephrology 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/760580.

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A growing body of evidence supports the concept that changes in the intrauterine milieu during “sensitive” periods of embryonic development or in infant diet after birth affect the developing individual, resulting in general health alterations later in life. This phenomenon is referred to as “developmental programming” or “developmental origins of health and disease.” The risk of developing late-onset diseases such as hypertension, chronic kidney disease (CKD), obesity or type 2 diabetes is increased in infants born prematurely at <37 weeks of gestation or in low birth weight (LBW) infants weighing <2,500 g at birth. Both genetic and environmental events contribute to the programming of subsequent risks of CKD and hypertension in premature or LBW individuals. A number of observations suggest that susceptibility to subsequent CKD and hypertension in premature or LBW infants is mediated, at least in part, by reduced nephron endowment. The major factors influencingin uteroenvironment that are associated with a low final nephron number include uteroplacental insufficiency, maternal low-protein diet, hyperglycemia, vitamin A deficiency, exposure to or interruption of endogenous glucocorticoids, and ethanol exposure. This paper discusses the effect of premature birth, LBW, intrauterine milieu, and infant feeding on the development of hypertension and renal disease in later life as well as examines the role of the kidney in developmental programming of hypertension and CKD.

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Plotnikova, Plotnikova E. Yu, Zakharova Yu V. Zakharova, Sinkova M. N. Sinkova, and Isakov L. K. Isakov. "Effects of probiotics on the intrauterine programming of infant microbiota." Akusherstvo i ginekologiia 9_2019 (September 30, 2019): 174–80. http://dx.doi.org/10.18565/aig.2019.9.174-180.

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Vedovato, S., S. Visentin, E. Cosmi, F. Cavallin, M. Mion, M. Zaninotto, D. Trevisanuto, and V. Zanardo. "1216 Intrauterine Growth Restriction and Developmental Programming of Renal Disease." Archives of Disease in Childhood 97, Suppl 2 (October 1, 2012): A347—A348. http://dx.doi.org/10.1136/archdischild-2012-302724.1216.

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Limesand, S. W. "737 Perinatal programming of pancreatic islets during intrauterine growth restriction." Journal of Animal Science 95, suppl_4 (August 1, 2017): 358. http://dx.doi.org/10.2527/asasann.2017.737.

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Ojeda, Norma B., Daniela Grigore, and Barbara T. Alexander. "Intrauterine Growth Restriction: Fetal Programming of Hypertension and Kidney Disease." Advances in Chronic Kidney Disease 15, no. 2 (April 2008): 101–6. http://dx.doi.org/10.1053/j.ackd.2008.01.001.

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Lanham, S. A., C. Roberts, M. J. Perry, C. Cooper, and R. O. C. Oreffo. "Intrauterine programming of bone. Part 2: Alteration of skeletal structure." Osteoporosis International 19, no. 2 (August 18, 2007): 157–67. http://dx.doi.org/10.1007/s00198-007-0448-3.

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Bertin, M., S. Visentin, M. Zaninotto, V. Zanardo, and E. Cosmi. "OP01.05: Intrauterine growth restriction and developmental programming of renal disease." Ultrasound in Obstetrics & Gynecology 40, S1 (September 2012): 56. http://dx.doi.org/10.1002/uog.11393.

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Lopez‐Tello, Jorge, Maria Arias‐Alvarez, Antonio Gonzalez‐Bulnes, and Amanda N. Sferuzzi‐Perri. "Models of Intrauterine growth restriction and fetal programming in rabbits." Molecular Reproduction and Development 86, no. 12 (September 20, 2019): 1781–809. http://dx.doi.org/10.1002/mrd.23271.

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Yajnik, Chittaranjan S., and Urmila S. Deshmukh. "Maternal nutrition, intrauterine programming and consequential risks in the offspring." Reviews in Endocrine and Metabolic Disorders 9, no. 3 (July 26, 2008): 203–11. http://dx.doi.org/10.1007/s11154-008-9087-z.

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Sallam, Nada, Victoria Palmgren, Radha Singh, Cini John, and Jennifer Thompson. "Programming of Vascular Dysfunction in the Intrauterine Milieu of Diabetic Pregnancies." International Journal of Molecular Sciences 19, no. 11 (November 20, 2018): 3665. http://dx.doi.org/10.3390/ijms19113665.

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With the rising global tide of obesity, gestational diabetes mellitus (GDM) burgeoned into one of the most common antenatal disorders worldwide. Macrosomic babies born to diabetic mothers are more likely to develop risk factors for cardiovascular disease (CVD) before they reach adulthood. Rodent studies in offspring born to hyperglycemic pregnancies show vascular dysfunction characterized by impaired nitric oxide (NO)-mediated vasodilation and increased production of contractile prostanoids by cyclooxygenase 2 (COX-2). Vascular dysfunction is a key pathogenic event in the progression of diabetes-related vascular disease, primarily attributable to glucotoxicity. Therefore, glucose-induced vascular injury may stem directly from the hyperglycemic intrauterine environment of GDM pregnancy, as evinced by studies showing endothelial activation and inflammation at birth or in childhood in offspring born to GDM mothers. This review discusses potential mechanisms by which intrauterine hyperglycemia programs dysfunction in the developing vasculature.

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