BULAŞICI OLMAYAN KRONİK HASTALIKLARDA FETAL PROGRAMLAMA
Year 2022,
Volume: 7 Issue: 3, 120 - 134, 23.12.2022
Gülben Karakuş
,
Teslime Özge Yörüsün
,
Duygu Ağagündüz
Abstract
İnsan vücudunda bir veya birden çok sistemin geri dönüşümsüz fonksiyon kaybı sonucunda ortaya çıkan ve yaşam boyu tedavi gerektiren kronik hastalıkların prevalansı dünyada giderek artmaktadır. İntrauterin ortamdaki fetüs sürekli bir gelişim halindedir. Fetüsün deoksiribonükleik asit (DNA) diziliminin fetal dö-nemde maruz kalınan maternal faktörlere ve çeşitli çevresel stresörlere bağlı olarak yeniden programlan-dığı belirtilmektedir. Fetal programlama hipotezine göre fetüsün maruz kaldığı stresler, yetişkinlik döne-mindeki kronik hastalıkların temelini oluşturmaktadır. Bu derlemede de dünyada yaygın görülen bulaşıcı olmayan kronik hastalıkların fetal programlaması ve programlamayı etkileyen bazı faktörler incelenmiştir.
References
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- 7.Özdemir K, Altınkaynak S, Çınar N. Fetal beslenmenin erişkin sağlığına etkileri. 2015; 24(2), 64-68.
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- 9. Staud F, Karahoda R. Trophoblast: The central unit of fetal growth, protection and programming. Int J Biochem Cell Biol. 2018; 105:35-40.
- 10. Lindsay KL, Buss C, Wadhwa PD, Entringer S. The interplay between nutrition and stress in pregnancy: implications for fetal programming of brain development. Biol Psychiatry. 2019; 85(2):135-149.
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- 21. Özer ÖF, Güler EM, Selek Ş, Çoban G, Türk HM, Koçyiğit A. Akciğer, meme ve kolon kanserli hastalarda oksidatif stres parametrelerinin değişimi. Harran Üniversitesi Tıp Fakültesi Dergisi. 2019; 16(2):235-240.
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- 26. Jebeile H, Kelly AS, O'Malley G, Baur LA. Obesity in children and adolescents: epidemiology, causes, assessment, and management. Lancet Diabetes Endocrinol. 2022; 10(5):351-365.
- 27. Kilinç F, Gözel N. Obezite Ve Genetik. Fırat Tıp Dergisi. 2018; 23:9-13.
- 28. Pi‐Sunyer FX. The obesity epidemic: pathophysiology and consequences of obesity. Obes Res. 2002; 10(12):97-104.
- 29. Slawik M, Beuschlein F. Genetics and pathophysiology of obesity. Internist (Berl). 2006; 47(2):120-129.
- 30. Butler MG. Single gene and syndromic causes of obesity: Illustrative examples. Prog Mol Biol Transl Sci. 2016; 140:1-45.
- 31. Semerci CN. Obezite ve genetik. Gülhane Tıp Dergisi. 2004; 46(4):353-359.
- 32. Pigeyre M, Meyre D. Monogenic Obesity in Pediatric Obesity. 2th Edition, Humana Press Cham, 2018; 135-152.
- 33. Marciniak A, et al. Fetal programming of the metabolic syndrome. Taiwan J Obstet Gynecol. 2017; 56(2):133-138.
- 34. Koenen M, Hill MA, Cohen P, Sowers JR. Obesity, adipose tissue and vascular dysfunction. Cir Res. 2021; 128(7):951-968.
- 35. Kawai T, Autieri MV, Scalia R. Adipose tissue inflammation and metabolic dysfunction in obesity. Am J Physiol Cell Physiol. 2021; 320(3):375-391.
- 36. Howell KR, Powell TL. Effects of maternal obesity on placental function and fetal development. Reproduction. 2017; 153(3):97-108.
- 37. Sapra A, Bhandari P, Wilhite A. Diabetes Mellitus (Nursing). StatPearls Publishing, Treasure Island (FL), 2021.
- 38.McCance DR, Pettitt DJ, Hanson RL, Jacobsson LT, Knowler WC, Bennett PH. Birth weight and non-insulin dependent diabetes, thrifty genotype, thrifty phenotype, or surviving small baby genotype?. BMJ. 1994; 308(6934):942-945.
- 39. Tomar AS, et al. Intrauterine programming of diabetes and adiposity. Curr Obes Rep. 2015; 4(4):418-428.
- 40. Krishnaveni GV, Yajnik C. Developmental origins of diabetes—an Indian perspective. Eur J Clin Nutr. 2017; 71(7):865-869.
- 41. Alexander BT, Dasinger JH, Intapad S. Fetal programming and cardiovascular pathology. Compr Physiol. 2015; 5(2):997.
- 42. Çimen H, Öztürk YE. Omega-3 Yağ Asitlerinin Kardiyovasküler Hastalıklar Üzerine Etkisi. Aydın Sağlık Dergisi 2022; 8(1):1-16.
- 43. Rosenfeld CS. The placenta‐brain‐axis. J Neurosci Res. 2021; 99(1):271-283.
- 44. Ortega MA, et al. The Pivotal Role of the Placenta in Normal and Pathological Pregnancies: A Focus on Preeclampsia, Fetal Growth Restriction, and Maternal Chronic Venous Disease. Cell. 2022; 11(3):568.
- 45. Burton GJ, Fowden AL, Thornburg KL. Placental origins of chronic disease. Physiol Rev. 2016; 96(4):1509-1565.
- 46. Shook LL, Kislal S, Edlow AG. Fetal brain and placental programming in maternal obesity: A review of human and animal model studies. Prenatal Diag. 2020; 40(9):1126-1137.
- 47. Yücel ÜÖ & Mutlu AA. Epigenetik Ve Böbrek Hastalıkları. Avrasya Sağlık Bilimleri Dergisi. 2020; 3(3):161-166.
- 48. Tain Y-L, Hsu C-N. Developmental origins of chronic kidney disease: should we focus on early life? Int J Mol Sci. 2017; 18(2):381.
- 49. Hsu C-N, Tain Y-L. Regulation of Nitric Oxide Production in the Developmental Programming of Hypertension and Kidney Disease. Int J Mol Sci. 2019; 20(3):681.
- 50. Stewart PM, et al. Hypertension in the syndrome of apparent mineralocorticoid excess due to mutation of the 11β-hydroxysteroid dehydrogenase type 2 gene. Lancet. 1996; 347(8994):88-91.
- 51. Li KX, Smith RE, Ferrari P, Funder JW, Krozowski ZS. Rat 11β-hydroxysteroid dehydrogenase type 2 enzyme is expressed at low levels in the placenta and is modulated by adrenal steroids in the kidney. Mol Cell Endocrinol. 1996; 120(1):67-75.
- 52. Rodríguez-Rodríguez P, et al. Implication of Oxidative Stress in Fetal Programming of Cardiovascular Disease. Front Physiol. 2018; 9(602):1-13.
- 53. Alexander BT. Fetal programming of hypertension. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2006; 290(1):1-10.
- 54. Çevik BA, Pirinçci E. Beslenme ve Kanser. Firat Tip Dergisi. 2017; 22(1):1-7.
- 55. Barker DJ, Thornburg KL. Placental programming of chronic diseases, cancer and lifespan: a review. Placenta. 2013; 34(10):841-845.
- 56. Ozanne SE, Fernandez-Twinn D, Hales CN. Fetal growth and adult diseases. Semin Perinatol. 2004; 28(1):81-87.
- 57. Kaur P, Shorey LE, Ho E, Dashwood RH, Williams DE. The epigenome as a potential mediator of cancer prevention by dietary phytochemicals: The fetus as a target. Nutr Rev. 2013; 71(7):441-457.
- 58. Azad M, et al. Diabetes in pregnancy and lung health in offspring: developmental origins of respiratory disease. Paediatr Respir Rev. 2017; 21:19-26.
- 59. Shi W, Bellusci S, Warburton D. Lung development and adult lung diseases. Chest. 2007; 132(2):651-656.
- 60. Davidson R, Roberts SE, Wotton CJ, Goldacre MJ. Influence of maternal and perinatal factors on subsequent hospitalisation for asthma in children: evidence from the Oxford record linkage study. Bmc Pulm Med. 2010;10(1):1-8.
FETAL PROGRAMMING IN NON-COMMUNICABLE CHRONIC DISEASES
Year 2022,
Volume: 7 Issue: 3, 120 - 134, 23.12.2022
Gülben Karakuş
,
Teslime Özge Yörüsün
,
Duygu Ağagündüz
Abstract
The prevalence of chronic diseases that occur as a result of irreversible loss of function of one or more systems in the human body and require lifelong treatment is increasing in the world. The fetus in the intra-uterine environment is in a state of continuous development. It is reported that the deoxyribonucleic acid (DNA) sequence of the fetus is reprogrammed depending on the maternal factors exposed during the fetal period and various environmental stressors. According to the fetal programming hypothesis, the stresses which the fetus exposed are the basis of chronic diseases in adulthood. In the present review, fetal pro-gramming of chronic non-communicable diseases that are common in the world and some factors affecting programming were examined.
References
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- 2.Kumsar AK, Yılmaz FT. Kronik Hastaliklarda Yaşam Kalitesine Genel Bakiş. Erü Sağlık Bilimleri Fakültesi Dergisi. 2014; 2(2):62-70.
- 3.Baysal A. Sağlıklı Beslenme: Uzmanların Önerisi Tüketicinin Algılaması. Beslenme ve Diyet Dergisi. 1998; 27(2):1-4.
- 4.Kartal FT, Helvaci G, Ayhan NY. Maternal Beslenme ve İlerleyen Yaşamda Obezite. Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi. 2020; 9(1):36-43.
- 5.Arslan S, Yıldıran H. Maternal Beslenmenin Yavrular Üzerine Etkileri: Fetal Programlama ve Epigenetik Mekanizmalar. Beslenme ve Diyet Dergisi. 2021; 49(1):67-74.
- 6.Godfrey KM, Barker DJ. Fetal nutrition and adult disease. Am J Clin Nutr. 2000; 71(5):1344S-1352S.
- 7.Özdemir K, Altınkaynak S, Çınar N. Fetal beslenmenin erişkin sağlığına etkileri. 2015; 24(2), 64-68.
- 8.Entringer S, de Punder K, Buss C, Wadhwa PD. The fetal programming of telomere biology hypothesis: an update. Philos Trans R Soc Lond B Biol Sci. 2018; 373(1741):20170151.
- 9. Staud F, Karahoda R. Trophoblast: The central unit of fetal growth, protection and programming. Int J Biochem Cell Biol. 2018; 105:35-40.
- 10. Lindsay KL, Buss C, Wadhwa PD, Entringer S. The interplay between nutrition and stress in pregnancy: implications for fetal programming of brain development. Biol Psychiatry. 2019; 85(2):135-149.
- 11. Mann FD, Cuevas AG, Krueger RF. Cumulative stress: A general “s” factor in the structure of stress. Soc Sci Med. 2021; 289:114405.
- 12. Nederhof E, Schmidt MV. Mismatch or cumulative stress: toward an integrated hypothesis of programming effects. Physiol Behav. 2012; 106(5):691-700.
- 13. van Bodegom M, Homberg JR, Henckens MJ. Modulation of the hypothalamic-pituitary-adrenal axis by early life stress exposure. Front Cell Neurosci. 2017; 11:87.
- 14. Conradt E, et al. Incorporating epigenetic mechanisms to advance fetal programming theories. Dev Psychopathol. 2018; 30(3):807-824.
- 15. Reynolds LP, et al. Developmental programming of fetal growth and development. Vet Clin North Am Food Anim Pract. 2019; 35(2):229-247.
- 16.Orcan S. Epigenetik ve epigenomik. Hacettepe Üniversitesi. 2006.
- 17. Merdol TK. DNA Metilasyonu ve Beslenme. Beslenme ve Diyet Dergisi. 2018; 46(2):103-106.
- 18. Güler C, Peynircioğlu BB. DNA metilasyonu ve hastalıklarla ilişkisi. Acıbadem Üniversitesi Sağlık Bilimleri Dergisi. 2016; (2):61-68.
- 19. Moreno-Fernandez J, Ochoa JJ, Lopez-Frias M, Diaz-Castro J. Impact of Early Nutrition, Physical Activity and Sleep on the Fetal Programming of Disease in the Pregnancy: A Narrative Review. Nutrients. 2020; 12(12):3900.
- 20. Özata M, Keservuran G. Metilasyonu Düzelt Sağlığına Kavuş. Editör: Özata M, Keservuran G. 1. baskı, Efe Akademi Yayınları, İstanbul, 2014.
- 21. Özer ÖF, Güler EM, Selek Ş, Çoban G, Türk HM, Koçyiğit A. Akciğer, meme ve kolon kanserli hastalarda oksidatif stres parametrelerinin değişimi. Harran Üniversitesi Tıp Fakültesi Dergisi. 2019; 16(2):235-240.
- 22. Yiğit A, Güneş F. Epigenetik Ve Tek Karbon Metabolizması: Folat Ve B12 Vitamininin Rolü. Türkiye Klinikleri Tip Bilimleri Dergisi. 2018; 3(3).
- 23. Şurgun E. Maternal Beslenmenin Epigenetik Mekanizmalar Üzerinden İnfant Sağliğina Etkileri. Başkent Üniversitesi Sağlık Bilimleri Fakültesi Dergisi-Büsbid. 2019; 4(1).
- 24.http://www.halksagligi.hacettepe.edu.tr/duyurular/halkayonelik/boh2019.pdf Erişim: 1 Temmuz, 2022
- 25. Teo KK, Rafiq T. Cardiovascular risk factors and prevention: a perspective from developing countries. Can J Cardiol. 2021; 37(5):733-743.
- 26. Jebeile H, Kelly AS, O'Malley G, Baur LA. Obesity in children and adolescents: epidemiology, causes, assessment, and management. Lancet Diabetes Endocrinol. 2022; 10(5):351-365.
- 27. Kilinç F, Gözel N. Obezite Ve Genetik. Fırat Tıp Dergisi. 2018; 23:9-13.
- 28. Pi‐Sunyer FX. The obesity epidemic: pathophysiology and consequences of obesity. Obes Res. 2002; 10(12):97-104.
- 29. Slawik M, Beuschlein F. Genetics and pathophysiology of obesity. Internist (Berl). 2006; 47(2):120-129.
- 30. Butler MG. Single gene and syndromic causes of obesity: Illustrative examples. Prog Mol Biol Transl Sci. 2016; 140:1-45.
- 31. Semerci CN. Obezite ve genetik. Gülhane Tıp Dergisi. 2004; 46(4):353-359.
- 32. Pigeyre M, Meyre D. Monogenic Obesity in Pediatric Obesity. 2th Edition, Humana Press Cham, 2018; 135-152.
- 33. Marciniak A, et al. Fetal programming of the metabolic syndrome. Taiwan J Obstet Gynecol. 2017; 56(2):133-138.
- 34. Koenen M, Hill MA, Cohen P, Sowers JR. Obesity, adipose tissue and vascular dysfunction. Cir Res. 2021; 128(7):951-968.
- 35. Kawai T, Autieri MV, Scalia R. Adipose tissue inflammation and metabolic dysfunction in obesity. Am J Physiol Cell Physiol. 2021; 320(3):375-391.
- 36. Howell KR, Powell TL. Effects of maternal obesity on placental function and fetal development. Reproduction. 2017; 153(3):97-108.
- 37. Sapra A, Bhandari P, Wilhite A. Diabetes Mellitus (Nursing). StatPearls Publishing, Treasure Island (FL), 2021.
- 38.McCance DR, Pettitt DJ, Hanson RL, Jacobsson LT, Knowler WC, Bennett PH. Birth weight and non-insulin dependent diabetes, thrifty genotype, thrifty phenotype, or surviving small baby genotype?. BMJ. 1994; 308(6934):942-945.
- 39. Tomar AS, et al. Intrauterine programming of diabetes and adiposity. Curr Obes Rep. 2015; 4(4):418-428.
- 40. Krishnaveni GV, Yajnik C. Developmental origins of diabetes—an Indian perspective. Eur J Clin Nutr. 2017; 71(7):865-869.
- 41. Alexander BT, Dasinger JH, Intapad S. Fetal programming and cardiovascular pathology. Compr Physiol. 2015; 5(2):997.
- 42. Çimen H, Öztürk YE. Omega-3 Yağ Asitlerinin Kardiyovasküler Hastalıklar Üzerine Etkisi. Aydın Sağlık Dergisi 2022; 8(1):1-16.
- 43. Rosenfeld CS. The placenta‐brain‐axis. J Neurosci Res. 2021; 99(1):271-283.
- 44. Ortega MA, et al. The Pivotal Role of the Placenta in Normal and Pathological Pregnancies: A Focus on Preeclampsia, Fetal Growth Restriction, and Maternal Chronic Venous Disease. Cell. 2022; 11(3):568.
- 45. Burton GJ, Fowden AL, Thornburg KL. Placental origins of chronic disease. Physiol Rev. 2016; 96(4):1509-1565.
- 46. Shook LL, Kislal S, Edlow AG. Fetal brain and placental programming in maternal obesity: A review of human and animal model studies. Prenatal Diag. 2020; 40(9):1126-1137.
- 47. Yücel ÜÖ & Mutlu AA. Epigenetik Ve Böbrek Hastalıkları. Avrasya Sağlık Bilimleri Dergisi. 2020; 3(3):161-166.
- 48. Tain Y-L, Hsu C-N. Developmental origins of chronic kidney disease: should we focus on early life? Int J Mol Sci. 2017; 18(2):381.
- 49. Hsu C-N, Tain Y-L. Regulation of Nitric Oxide Production in the Developmental Programming of Hypertension and Kidney Disease. Int J Mol Sci. 2019; 20(3):681.
- 50. Stewart PM, et al. Hypertension in the syndrome of apparent mineralocorticoid excess due to mutation of the 11β-hydroxysteroid dehydrogenase type 2 gene. Lancet. 1996; 347(8994):88-91.
- 51. Li KX, Smith RE, Ferrari P, Funder JW, Krozowski ZS. Rat 11β-hydroxysteroid dehydrogenase type 2 enzyme is expressed at low levels in the placenta and is modulated by adrenal steroids in the kidney. Mol Cell Endocrinol. 1996; 120(1):67-75.
- 52. Rodríguez-Rodríguez P, et al. Implication of Oxidative Stress in Fetal Programming of Cardiovascular Disease. Front Physiol. 2018; 9(602):1-13.
- 53. Alexander BT. Fetal programming of hypertension. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2006; 290(1):1-10.
- 54. Çevik BA, Pirinçci E. Beslenme ve Kanser. Firat Tip Dergisi. 2017; 22(1):1-7.
- 55. Barker DJ, Thornburg KL. Placental programming of chronic diseases, cancer and lifespan: a review. Placenta. 2013; 34(10):841-845.
- 56. Ozanne SE, Fernandez-Twinn D, Hales CN. Fetal growth and adult diseases. Semin Perinatol. 2004; 28(1):81-87.
- 57. Kaur P, Shorey LE, Ho E, Dashwood RH, Williams DE. The epigenome as a potential mediator of cancer prevention by dietary phytochemicals: The fetus as a target. Nutr Rev. 2013; 71(7):441-457.
- 58. Azad M, et al. Diabetes in pregnancy and lung health in offspring: developmental origins of respiratory disease. Paediatr Respir Rev. 2017; 21:19-26.
- 59. Shi W, Bellusci S, Warburton D. Lung development and adult lung diseases. Chest. 2007; 132(2):651-656.
- 60. Davidson R, Roberts SE, Wotton CJ, Goldacre MJ. Influence of maternal and perinatal factors on subsequent hospitalisation for asthma in children: evidence from the Oxford record linkage study. Bmc Pulm Med. 2010;10(1):1-8.