Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood
Jazyk angličtina Země Velká Británie, Anglie Médium electronic
Typ dokumentu časopisecké články, přehledy
PubMed
26787358
PubMed Central
PMC4719732
DOI
10.1186/s12929-016-0233-8
PII: 10.1186/s12929-016-0233-8
Knihovny.cz E-zdroje
- MeSH
- epigeneze genetická * MeSH
- kardiovaskulární systém embryologie patologie MeSH
- kuchyňská sůl * MeSH
- lidé MeSH
- renin-angiotensin systém * MeSH
- růstová retardace plodu metabolismus patologie MeSH
- těhotenství MeSH
- vývojová regulace genové exprese * MeSH
- zpožděný efekt prenatální expozice metabolismus patologie MeSH
- Check Tag
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- kuchyňská sůl * MeSH
Recent studies reported the critical role of the intrauterine environment of a fetus in growth or the development of disease in adulthood. In this article we discussed the implications of salt restriction in growth of a fetus and the development of growth-related disease in adulthood. Salt restriction causes retardation of fatal growth or intrauterine death thereby leading to low birth weight or decreased birth rate. Such retardation of growth along with the upregulation of the renin angiotensin system due to salt restriction results in the underdevelopment of cardiovascular organs or decreases the number of the nephron in the kidney and is responsible for onset of hypertension in adulthood. In addition, gestational salt restriction is associated with salt craving after weaning. Moreover, salt restriction is associated with a decrease in insulin sensitivity. A series of alterations in metabolism due to salt restriction are probably mediated by the upregulation of the renin angiotensin system and an epigenetic mechanism including proinflammatory substances or histone methylation. Part of the metabolic disease in adulthood may be programmed through such epigenetic changes. The modification of gene in a fetus may be switched on through environment factors or life style after birth. The benefits of salt restriction have been assumed thus far; however, more precise investigation is required of its influence on the health of fetuses and the onset of various diseases in adulthood.
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Raymond R, Townsend RR, Wilkinson IB, Schiffrin EL, Avolio AP, Chirinos JA, et al. Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement From the American Heart Association. Hypertension. 2015;66:698–722. doi: 10.1161/HYP.0000000000000033. PubMed DOI PMC
Mozaffarian D, Fahimi S, Singh GM, Micha R, Khatibzadeh S, Engell RE, et al. Global Burden of Diseases Nutrition and Chronic Diseases Expert Group. Global sodium consumption and death from cardiovascular causes. N Engl J Med. 2014;371:624–34. doi: 10.1056/NEJMoa1304127. PubMed DOI
Fulgoni VL, Agarwal S, Lisa Spence L, Samuel P. Sodium intake in US ethnic subgroups and potential impact of a new sodium reduction technology: NHANES Dietary Modeling. Nutr J. 2014;13:120. doi: 10.1186/1475-2891-13-120. PubMed DOI PMC
The Salt Industry Center of Japan. Trends of salt intake in Japan (in Japanese). http://www.shiojigyo.com/a080data/img/sessyuryou24.pdf
Rapp JP. Dahl salt-susceptible and salt-resistant rats. Hypertension. 1982;4:753–63. doi: 10.1161/01.HYP.4.6.753. PubMed DOI
Dahl LK. Effects of chronic excessive salt feeding. Induction of self sustaining hypertension in rats. J Exp Med. 1961;114:231–6. doi: 10.1084/jem.114.2.231. PubMed DOI PMC
McLean R, Williams S, Mann J. Monitoring population sodium intake using spot urine samples: validation in a New Zealand population. J Hum Hypertens. 2014;28:657–62. doi: 10.1038/jhh.2014.10. PubMed DOI
Hawkes C, Webster J. National Approaches to Monitoring Population Salt Intake: A Trade-Off between Accuracy and Practicality? PLOS one. 2012;7 doi: 10.1371/journal.pone.0046727. PubMed DOI PMC
Mente A, O’Donnell M, Yusuf S. Extreme sodium reductions for the entire population: Zealotry or Evidence Based? Am J Hypertens. 2013;26:1187–90. doi: 10.1093/ajh/hpt148. PubMed DOI
Graudal N, Jurgens G, Baslund B, Alderman MH. Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis. Am J Hypertens. 2014;27:1129–37. doi: 10.1093/ajh/hpu028. PubMed DOI
O’Donnell M, Mente A, Rangarajan S, McQueen MJ, Wang X, Liu L, PURE Investigators et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014;371:612–23. doi: 10.1056/NEJMoa1311889. PubMed DOI
Mente A, O’Donnell MJ, Rangarajan S, McQueen MJ, Poirier P, Wielgosz A, PURE Investigators et al. Association of urinary sodium and potassium excretion with blood pressure. N Engl J Med. 2014;371:601–11. doi: 10.1056/NEJMoa1311989. PubMed DOI
Chou R, Hara A, Du DD, Shimizu N, Sakuyama H, Uehara Y. Low salt intake during pregnancy is associated with low birth rate and low survival rate in rats with salt-sensitivity. J Nutr Met. Volume 2014. Article ID 212089, 5 pages. doi:10.1155/2014/212089 PubMed PMC
Feeds for laboratory animals. Bioresearch Services by Oriental Yeast Co., Ltd., Tokyo, Japan; 2011
de Siqueira FR, de Souza RM, de Oliveira IB, Furukawa LNS, Heimann JC. Low sodium intake is associated with low birth weight and size only when given in the second half of gestation. The FASEB J. 2012;26:712.4.
Crystal SR, Bernstein IL. Morning sickness: impact on offspring salt preference. Appetite. 1995;25:231–40. doi: 10.1006/appe.1995.0058. PubMed DOI
Crystal SR, Bowen DJ, Bernstein IL. Morning sickness and salt intake, food cravings, and food aversions. Physiol Behav. 1996;67:181–7. doi: 10.1016/S0031-9384(99)00055-4. PubMed DOI
Crystal SR, Bernstein IL. Infant salt preference and mother's morning sickness. Appetite. 1998;30:297–307. doi: 10.1006/appe.1997.0144. PubMed DOI
Shirazki A, Weintraub Z, Reich D, Gershon E, Leshem M. Lowest neonatal serum sodium predicts sodium intake in low birth weight children. Am J Physiol Regul Integr Comp Physiol. 2007;292:R1683–9. doi: 10.1152/ajpregu.00453.2006. PubMed DOI
Leshem M. Salt preference in adolescence is predicted by common prenatal and infantile mineralofluid loss. Physiol Behav. 1998;63:699–704. doi: 10.1016/S0031-9384(97)00525-8. PubMed DOI
Nicolaidis S, Galaverna O, Metzler CH. Extracellular dehydration during pregnancy increases salt appetite of offspring. Am J Physiol. 1990;258:R281–3. PubMed
Galaverna O, Nicolaïdis S, Yao SZ, Sakai RR, Epstein AN. Endocrine consequences of prenatal sodium depletion prepare rats for high need-free NaCl intake in adulthood. Am J Physiol. 1995;269:R578–83. PubMed
Hara A, Chou R, Sakuyama H, Du DD, Uehara Y. Low salt diet in pregnant mothers is associated with enhanced salt appetite in their offspring of Dahl salt-sensitive rats. Food Nutr Sci. 2014;5:1904–13. doi: 10.4236/fns.2014.519202. DOI
Kresser C. Why low-salt diets are dangerous during pregnancy. http://healthybabycode.com/why-low-salt-diets-are-dangerous-during-pregnancy. Low-salt diet increases insulin resistance in healthy subjects. 2015 March.
Leandro SM, Furukawa LNS, Shimizu MHM, Casarini DE, Seguro AC, Patriarca G, et al. Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin-angiotensin system. Physiol Behav. 2008;95:145–51. doi: 10.1016/j.physbeh.2008.05.011. PubMed DOI
Bursey RG, Watson ML. The effect of sodium restriction during gestation on offspring brain development in rat. Am J Clin Nutr. 1983;37:43–51. PubMed
Brosnihan KB, Hering L, Dechend R, Chappell MC, Herse F. Increased angiotensin II in the mesometrial triangle of a transgenic rat model of preeclampsia. Hypertension. 2010;55:562–6. doi: 10.1161/HYPERTENSIONAHA.109.145656. PubMed DOI PMC
Anton L, Merrill DC, Neves LA, Diz D, Corthorn J, Valdes G, et al. The uterine placental bed renin-angiotensin system in normal and preeclamptic pregnancy. Endocrinology. 2009;150:4316–25. doi: 10.1210/en.2009-0076. PubMed DOI PMC
Shah DM. The role of RAS in the pathogenesis of preeclampsia. Curr Hypertens Rep. 2006;8:144–52. doi: 10.1007/s11906-006-0011-1. PubMed DOI
Kato M, Natarajan R. Diabetic nephropathy-emerging epigenetic mechanisms. Nat Rev Nephrol. 2014;10:517–30. doi: 10.1038/nrneph.2014.116. PubMed DOI PMC
Song R, Van Buren T, Yosypiv IV. Histone deacetylases are critical regulators of the renin-angiotensin system during ureteric bud branching morphogenesis. Pediatr Res. 2010;67:573–8. doi: 10.1203/PDR.0b013e3181da477c. PubMed DOI PMC
Goyal R, Goyal D, Leitzke A, Gheorghe CP, Longo LD. Brain renin-angiotensin system: fetal epigenetic programming by maternal protein restriction during pregnancy. Reprod Sci. 2010;17:227–38. doi: 10.1177/1933719109351935. PubMed DOI
Reddy MA, Sumanth P, Lanting L, Yuan H, Wang M, Mar D, et al. Losartan reverses permissive epigenetic changes in renal glomeruli of diabetic db/db mice. Kidney Int. 2014;85:362–73. doi: 10.1038/ki.2013.387. PubMed DOI PMC
Guan J, Mao C, Feng X, Zhang H, Xu F, Geng C, et al. Fetal development of regulatory mechanisms for body fluid homeostasis. Brazil J Med Biol Res. 2008;41:446–54. doi: 10.1590/S0100-879X2008005000025. PubMed DOI
van der Post JAM, van Buul BJA, Hart AAM, van Heerikhuize JJ, Pesman G, Legros JJ, et al. Vasopressin and oxytocin levels during normal pregnancy: effects of chronic dietary sodium restriction. J Endocrinol. 1997;152:345–54. doi: 10.1677/joe.0.1520345. PubMed DOI
Barker DJP, Osmond C, Winter PD, Margetts B, Simmonds SJ. Weight in infancy and death from ischemic heart disease. Lancet. 1989;2:577–80. doi: 10.1016/S0140-6736(89)90710-1. PubMed DOI
Vidonho AF, Jr, da Silva AA, Catanozi S, Rocha JC, Beutel A, Carillo BA, et al. Perinatal salt restriction: a new pathway to programming insulin resistance and dyslipidemia in adult Wistar rats. Pediatr Res. 2004;56:842–8. doi: 10.1203/01.PDR.0000145258.75160.5B. PubMed DOI
Lopes KL, Furukawa LNS, de Oliveira IB, Dolnikoff MS, Heimann JC. Perinatal salt restriction: a new pathway to programming adiposity indices in adult female Wistar rats. Life Sci. 2008;82:728–32. doi: 10.1016/j.lfs.2008.01.003. PubMed DOI
Dalziel SR, Parag V, Rodgers A, Harding JE. Cardiovascular risk factors at age 30 following preterm birth. Int J Epidemiol. 2007;36:907–15. doi: 10.1093/ije/dym067. PubMed DOI
Uiterwaal CS, Anthony S, Launer LJ, Witteman JC, Trouwborst AM, Hofman A, et al. Birth weight, growth, and blood pressure: an annual follow-up study of children aged 5 through 21 years. Hypertension. 1997;30:267–71. doi: 10.1161/01.HYP.30.2.267. PubMed DOI
Adair L, Dahly D. Developmental determinants of blood pressure in adults. Annu Rev Nutr. 2005;25:407–34. doi: 10.1146/annurev.nutr.25.050304.092538. PubMed DOI
Barker DJP, Eriksson JG, Forsen T, Osmond C. Fetal origins of adult disease: strength of effects and biological basis. Int J Epidemiol. 2002;31:1235–9. doi: 10.1093/ije/31.6.1235. PubMed DOI
Benz K, Amann K. Maternal nutrition, low nephron number and arterial hypertension in later life. Biochim Biophys Acta. 1802;2010:1309–17. PubMed
Moritz KM, Mazzuca MQ, Siebel AL, Mibus A, Arena D, Tare M, et al. Uteroplacntal insufficieny causes a nephron deficit, modest renal insufficiency but no hypertension with ageing in female rats. J Physiol. 2009;587:2635–46. doi: 10.1113/jphysiol.2009.170407. PubMed DOI PMC
Baum M. Role of the kidney in the prenatal and early postnatal programing of hypertension. Am J Physiol Renal Physiol. 2010;298:F235–7. doi: 10.1152/ajprenal.00288.2009. PubMed DOI PMC
Simonnetti GD, Raio L, Surbek D, Nelle M, Frey FJ, Mohaupt MG. Salt sensitivity of children with low birth weight. Hypertension. 2008;52:625–30. doi: 10.1161/HYPERTENSIONAHA.108.114983. PubMed DOI
Mecawia AS, Macchionec AF, Nuñeze P, Perillane C, Reisa LC, Vivasc L, et al. Arguellese J. Developmental programing of thirst and sodium appetite. Neurosci Biobehav Rev. 2015;51:1–14. doi: 10.1016/j.neubiorev.2014.12.012. PubMed DOI
Sasaki M, Yamada K, Namba H, Yoshinaga M, Du D, Uehara Y. Angiotensinogen gene polymorphisms and food-intake behavior in young, normal female subjects in Japan. Nutrition. 2013;29:60–5. doi: 10.1016/j.nut.2012.03.013. PubMed DOI
Yang W, Mao C, Xia F, Zheng A, Zhu L, He R, et al. Changed salt appetite and central angiotensin II-induced cellular activation in rat offspring following hypoxia during fetal stages. Peptides. 2010;31:1177–83. doi: 10.1016/j.peptides.2010.03.009. PubMed DOI PMC
Nakano-Tateno T, Shichiri M, Suzuki-Kemuriyama N, Tani Y, Izumiyama H, Hirata Y. Prolonged effects of intracerebroventricular angiotensin II on drinking, eating and locomotor behavior in mice. Regul Peptides. 2012;173:86–92. doi: 10.1016/j.regpep.2011.09.011. PubMed DOI
Mecawi AS, Araujo IG, Rocha FF, Coimbra TM, Antunes-Rodrigues J, Reis LC. Ontogenetic role of angiotensin-converting enzyme in rats: thirst and sodium appetite evaluation. Physiol Behav. 2010;99:118–24. doi: 10.1016/j.physbeh.2009.10.018. PubMed DOI
Bader M. Tissue renin-angiotensin-aldosterone systems: targets for pharmacological therapy. Annu Rev Pharmacol Toxicol. 2010;50:439–65. doi: 10.1146/annurev.pharmtox.010909.105610. PubMed DOI
Kingdom JC, Hayes M, McQueen J, Howatson AG, Lindop GB. Intrauterine growth restriction is associated with persistent juxtamedullary expression of renin in the fetal kidney. Kidney Int. 1999;55:424–9. doi: 10.1046/j.1523-1755.1999.00295.x. PubMed DOI
Kingdom JC, McQueen J, Connell JM, Whittle MJ. Fetal angiotensin II levels and vascular (type I) angiotensin receptors in pregnancies complicated by intrauterine growth retardation. Br J Obstet Gynaecol. 1993;100:476–82. doi: 10.1111/j.1471-0528.1993.tb15276.x. PubMed DOI
Antoes L, Merrill DC, Neves LAA, Diz DI, Corthorn J, Valdes G, et al. The uterine placental bed renin-angiotensin system in normal and preeclamptic pregnancy. Endocrinology. 2009;150:4316–25. doi: 10.1210/en.2009-0076. PubMed DOI PMC
Shah DM. The role of RAS in the pathogenesis of preeclampsia. Curr Hypetens Rep. 2006;8:144–52. doi: 10.1007/s11906-006-0011-1. PubMed DOI
Svitok P, Molcan L, Vesela A, Kruzliak P, Moravcik R, Zeman M. Increased salt intake during early ontogenesis lead to development of arterial hypertension in salt-resistant Wistar rats. Clin Exp Hypertens. 2015;37:142–7. doi: 10.3109/10641963.2014.913610. PubMed DOI
Lumbers ER. Functions of the renin–angiotensin system during development. Clin Exp Pharm Physiol. 1995;22:499–505. doi: 10.1111/j.1440-1681.1995.tb02057.x. PubMed DOI
Tabacova SA, Kimmel CA. Enalapril: pharmacokinetic/dynamic inferences for comparative developmental toxicity. A review. Reprod Toxicol. 2001;15:467–78. doi: 10.1016/S0890-6238(01)00161-7. PubMed DOI
Vehaskari VM, Aviles DH, Manning J. Prenatal programming of adult hypertension in the rat. Kidney Int. 2001;59:238–45. doi: 10.1046/j.1523-1755.2001.00484.x. PubMed DOI
Matsusaka T, Miyazaki Y, Ichikawa I. The renin angiotensin system and kidney development. Annu Rev Physiol. 2002;64:551–61. doi: 10.1146/annurev.physiol.64.081501.155721. PubMed DOI
Woods LL. Fetal origins of adult hypertension: a renal mechanism? Curr Opin Nephrol Hypertens. 2000;9:419–25. doi: 10.1097/00041552-200007000-00014. PubMed DOI
Garg R, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK. Low-salt diet increases insulin resistance in healthy subjects. Metabolism. 2011;60:965–8. doi: 10.1016/j.metabol.2010.09.005. PubMed DOI PMC
Klimas J, Olvedy M, Ochodnicka-Mackovicova K, Kruzliak P, Cacanyiova S, Kristek F, et al. Perinatally administered losartan augments renal ACE2 expression but not cardiac or renal Mas receptor in spontaneously hypertensive rats. J Cell Mol Med. 2015;19:1965–74. doi: 10.1111/jcmm.12573. PubMed DOI PMC
Rotteveel J, van Weissenbruch MM, Twisk JW. Delemarre-Van de Waal HA. Infant and childhood growth patterns, insulin sensitivity, and blood pressure in prematurely born young adults. Pediatrics. 2008;122:313–21. doi: 10.1542/peds.2007-2012. PubMed DOI
Hovi P, Andersson S, Eriksso JG, Järvenpää AL, Strang-Karlsson S, Mäkitie O, et al. Glucose regulation in young adults with very low birth weight. N Engl J Med. 2007;356:2053–63. doi: 10.1056/NEJMoa067187. PubMed DOI
Reid IA, Morris BJ, Ganong WF. The Renin-Angiotensin System. Annu Rev Physiol. 1978;40:377–410. doi: 10.1146/annurev.ph.40.030178.002113. PubMed DOI
Güllner HG. Regulation of sodium and water excretion by catecholamines. Life Sci. 1983;32:921–5. doi: 10.1016/0024-3205(83)90920-7. PubMed DOI
Gesek FA. Stimulation of alpha 2-adrenergic receptors increases Na(+)-K(+)-ATPase activity in distal convoluted tubule cells. Am J Physiol. 1993;265:F561–8. PubMed
Lönnqvist F, Thöme A, Nilsell K, Hoffstedt J, Arner PJ. A pathogenic role of visceral fat beta 3-adrenoceptors in obesity. Clin Invest. 1995;95:1109–16. doi: 10.1172/JCI117758. PubMed DOI PMC
Sakane N, Yoshida T, Umekawa T, Kondo M, Sakai Y, Takahashi T. Beta 3-adrenergic-receptor polymorphism: a genetic marker for visceral fat obesity and the insulin resistance syndrome. Diabetologia. 1997;40:200–4. doi: 10.1007/s001250050663. PubMed DOI
García-Rubi E, Calles-Escandón J. Insulin resistance and type 2 diabetes mellitus: its relationship with the beta 3-adrenergic receptor. Arch Med Res. 1999;30:459–64. doi: 10.1016/S0188-4409(99)00077-6. PubMed DOI
Ruivo GF, Leandro SM, do Nascimento CA, Catanozi S, Rocha JC, Furukawa LN, et al. Insulin resistance due to chronic salt restriction is corrected by alpha and beta blockade and by L-arginine. Physiol Behav. 2006;88:364–70. doi: 10.1016/j.physbeh.2006.04.006. PubMed DOI
Johansson S, Norman M, Legnevall L, Dalmaz Y, Lagercrantz H, Vanpée M. Increased catecholamines and heart rate in children with low birth weight: perinatal contributions to sympathoadrenal overactivity. J Intern Med. 2007;261:480–7. doi: 10.1111/j.1365-2796.2007.01776.x. PubMed DOI
Kamide K. Role of renin-angiotensin-aldosterone system in metabolic syndrome and obesity-related hypertension. Curr Hypertens Rev. 2014;9:238–45. doi: 10.2174/1573402110666140812122349. PubMed DOI
Frigolet ME, Torres N, Tovar AR. The renin-angiotensin system in adipose tissue and its metabolic consequences during obesity. J Nutr Biochem. 2013;24:2003–15. doi: 10.1016/j.jnutbio.2013.07.002. PubMed DOI
de Kloet AD, Krause EG, Woods SC. The renin angiotensin system and the metabolic syndrome. Physiol Behav. 2010;100:525–34. doi: 10.1016/j.physbeh.2010.03.018. PubMed DOI PMC
Olefsky JM, Glass CK. Macrophages, inflammation, and insulin resistance. Ann Rev Physiol. 2010;72:219–46. doi: 10.1146/annurev-physiol-021909-135846. PubMed DOI
Blüher M, Kratzsch J, Paschke R. Plasma levels of tumor necrosis factor-alpha, angiotensin II, growth hormone, and IGF-I are not elevated in insulin-resistant obese individuals with impaired glucose tolerance. Diabetes Care. 2001;24:328–34. doi: 10.2337/diacare.24.2.328. PubMed DOI
de Vinuesa SG, Goicoechea M, Kanter J, Puerta M, Cachofeiro V, Lahera V, et al. Insulin resistance, inflammatory biomarkers, and adipokines in patients with chronic kidney disease: effects of angiotensin II blockade. J Am Soc Nephrol. 2006;17:S206–12. doi: 10.1681/ASN.2006080916. PubMed DOI
Wei Y, Sowers JR, Clark SE, Li W, Ferrario CM, Stump CS. Angiotensin II-induced skeletal muscle insulin resistance mediated by NF-kappaB activation via NADPH oxidase. Am J Physiol Endocrinol Metab. 2008;294:E345–51. doi: 10.1152/ajpendo.00456.2007. PubMed DOI
Fasshauer M, Klein J, Neumann S, Eszlinger M, Paschke R. Tumor necrosis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes. Biochem Biophys Res Commun. 2001;288:1027–31. doi: 10.1006/bbrc.2001.5874. PubMed DOI
Fortuño A, Bidegain J, Robador PA, Hermida J, López-Sagaseta J, Beloqui O, et al. Losartan metabolite EXP3179 blocks NADPH oxidase-mediated superoxide production by inhibiting protein kinase C: potential clinical implications in hypertension. Hypertension. 2009;54:744–50. doi: 10.1161/HYPERTENSIONAHA.109.129353. PubMed DOI
Okamoto MM, Sumida DH, Carvaho CRO, Vargas AM, Heimann JC, Schaan BDA, et al. Changes in dietary sodium consumption modulate GLUT4 gene expression and early steps of insulin signaling. Am J Physiol Regul Integr Comp Physiol. 2004;286:R779–85. doi: 10.1152/ajpregu.00396.2003. PubMed DOI
Prada PO, Coelho MS, Zecchin HG, Dolnikoff MS, Gasparetti AL, Furukawa LN, et al. Low salt intake modulates insulin signaling, JNK activity and IRS-1 ser307 phosphorylation in rat tissues. J Endocrinol. 2005;185:429–37. doi: 10.1677/joe.1.06028. PubMed DOI
Liotto N, Miozzo M, Giannì ML, Taroni F, Morlacchi L, Piemontese P, et al. Early nutrition: the role of genetics and epigenetics. Pediatr Med Chir. 2009;31:65–71. PubMed
Zinkhan EK, Fu Q, Wang Y, Yu X, Callaway CW, Segar JL, et al. Maternal hyperglycemia disrupts histone 3 lysine 36 trimethylation of the IGF-1 gGene. J Nutr Metab. 2012;2012:930364. doi: 10.1155/2012/930364. PubMed DOI PMC
Fu Q, McKnight RA, Callaway CW, Yu X, Lane RH, Majnik AV. Intrauterine growth restriction disrupts developmental epigenetics around distal growth hormone response elements on the rat hepatic IGF-1 gene. FASEB J. 2015;29:1176–84. doi: 10.1096/fj.14-258442. PubMed DOI
Fu Q, Yu X, Callaway CW, Lane RH, McKnight RA. Epigenetics: intrauterine growth retardation (IUGR) modifies the histone code along the rat hepatic IGF-1 gene. FASEB J. 2009;23:2438–49. doi: 10.1096/fj.08-124768. PubMed DOI PMC
Touyz RM, Tabet F, Schiffrin EL. Redox-dependent signalling by angiotensin II and vascular remodeling in hypertension. Clin Exp Pharmacol Physiol. 2003;30:860–6. doi: 10.1046/j.1440-1681.2003.03930.x. PubMed DOI
Touyz RM, Yao G, Viel E, Amiri F, Schiffrin EL. Angiotensin II and endothelin-1 regulate MAP kinases through different redox-dependent mechanisms in human vascular smooth muscle cells. J Hypertens. 2004;22:1141–9. doi: 10.1097/00004872-200406000-00015. PubMed DOI
Paravicini TM, Touyz RM. Redox signaling in hypertension. Cardiovasc Res. 2006;1:247–58. doi: 10.1016/j.cardiores.2006.05.001. PubMed DOI