nach oben

Die Diabetologie

Erschienen in:

07.09.2016 | Typ-2-Diabetes | CME

Perinatale Programmierung des Typ-2-Diabetes

verfasst von: R. Ensenauer, E. Hucklenbruch-Rother, V. Brüll, Prof. Dr. J. Dötsch

Erschienen in: Die Diabetologie | Ausgabe 6/2016

Einloggen, um Zugang zu erhalten

Zusammenfassung

Über Mechanismen der sog. fetalen Programmierung erhöhen bereits Einflüsse in utero das Risiko der Nachkommen, im späteren Leben metabolische Dysbalancen wie Typ-2-Diabetes zu entwickeln. Wesentliche Risikofaktoren hierfür sind die intrauterine Wachstumsrestriktion, eine präkonzeptionelle mütterliche Adipositas und eine diabetische Stoffwechsellage während der Schwangerschaft. Der materne Diabetes mellitus selbst beeinflusst die Organfunktion der Nachkommen auf vielfältige Weise und langfristig. Bei den zugrunde liegenden Mechanismen der perinatalen Programmierung ist von epigenetischen Prozessen auszugehen. Diese können funktionelle (Genexpressionsebene) und/oder strukturelle Veränderungen (Organmorphologie) bei den Nachkommen bedingen. Eine detailliertere Kenntnis der perinatalen Ursachen für die Entstehung von Diabetes mellitus Typ 2 und seiner Vorstadien ist für die Entwicklung präventiver Konzepte und früher Behandlungsmaßnahmen von enormer Bedeutung.

Dabelea D, Mayer-Davis EJ, Saydah S et al (2014) Prevalence of type 1 and type 2 diabetes among children and adolescents from 2001 to 2009. JAMA 311:1778–1786CrossRefPubMedPubMedCentral

May AL, Kuklina EV, Yoon PW (2012) Prevalence of cardiovascular disease risk factors among US adolescents, 1999–2008. Pediatrics 129:1035–1041CrossRefPubMed

Kurth BM, Schaffrath Rosario A (2010) Overweight and obesity in children and adolescents in Germany. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz 53:643–652CrossRefPubMed

Hagman E, Reinehr T, Kowalski J et al (2014) Impaired fasting glucose prevalence in two nationwide cohorts of obese children and adolescents. Int J Obes (Lond) 38:40–45CrossRef

Rhodes ET, Prosser LA, Hoerger TJ et al (2012) Estimated morbidity and mortality in adolescents and young adults diagnosed with Type 2 diabetes mellitus. Diabet Med 29:453–463CrossRefPubMed

White NH (2015) Long-term outcomes in youths with diabetes mellitus. Pediatr Clin North Am 62:889–909CrossRefPubMedPubMedCentral

Nehring I, Von Kries R, Ensenauer R (2013) Perinatale Determinanten. In: Wirth A, Hauner H (Hrsg) Adipositas: Ätiologie, Folgekrankheiten, Diagnostik, Therapie. Springer, Heidelberg, S 56–59

Ravelli AC, Van Der Meulen JH, Michels RP et al (1998) Glucose tolerance in adults after prenatal exposure to famine. Lancet 351:173–177CrossRefPubMed

Ozanne SE, Jensen CB, Tingey KJ et al (2005) Low birthweight is associated with specific changes in muscle insulin-signalling protein expression. Diabetologia 48:547–552CrossRefPubMed

10.

Whincup PH, Kaye SJ, Owen CG et al (2008) Birth weight and risk of type 2 diabetes: A systematic review. JAMA 300:2886–2897CrossRefPubMed

11.

Mericq V, Ong KK, Bazaes R et al (2005) Longitudinal changes in insulin sensitivity and secretion from birth to age three years in small- and appropriate-for-gestational-age children. Diabetologia 48:2609–2614CrossRefPubMed

12.

Mingrone G, Manco M, Mora ME et al (2008) Influence of maternal obesity on insulin sensitivity and secretion in offspring. Diabetes Care 31:1872–1876CrossRefPubMedPubMedCentral

13.

Catalano PM, Presley L, Minium J et al (2009) Fetuses of obese mothers develop insulin resistance in utero. Diabetes Care 32:1076–1080CrossRefPubMedPubMedCentral

14.

Whitaker RC (2004) Predicting preschooler obesity at birth: The role of maternal obesity in early pregnancy. Pediatrics 114:e29–e36CrossRefPubMed

15.

Ensenauer R, Chmitorz A, Riedel C et al (2013) Effects of suboptimal or excessive gestational weight gain on childhood overweight and abdominal adiposity: Results from a retrospective cohort study. Int J Obes (Lond) 37:505–512CrossRef

16.

Ogonowski J, Miazgowski T, Kuczynska M et al (2009) Pregravid body mass index as a predictor of gestational diabetes mellitus. Diabet Med 26:334–338CrossRefPubMed

17.

Silverman BL, Metzger BE, Cho NH et al (1995) Impaired glucose tolerance in adolescent offspring of diabetic mothers. Relationship to fetal hyperinsulinism. Diabetes Care 18:611–617CrossRefPubMed

18.

Pedersen J (1952) Diabetes and pregnancy: Blood sugar of newborn infants (Ph.D. Thesis). Danish Science Press, Copenhagen, S 230

19.

Fraser A, Lawlor DA (2014) Long-term health outcomes in offspring born to women with diabetes in pregnancy. Curr Diab Rep 14:489CrossRefPubMedPubMedCentral

20.

Group HSCR, Metzger BE, Lowe LP et al (2008) Hyperglycemia and adverse pregnancy outcomes. N Engl J Med 358:1991–2002CrossRef

21.

Ensenauer R, Brandlhuber L, Burgmann M et al (2015) Obese nondiabetic pregnancies and high maternal Glycated hemoglobin at delivery as an indicator of offspring and maternal postpartum risks: The Prospective PEACHES Mother-Child Cohort. Clin Chem 61:1381–1390CrossRefPubMed

22.

Bunt JC, Tataranni PA, Salbe AD (2005) Intrauterine exposure to diabetes is a determinant of hemoglobin A(1)c and systolic blood pressure in pima Indian children. J Clin Endocrinol Metab 90:3225–3229CrossRefPubMedPubMedCentral

23.

Nelson RG, Morgenstern H, Bennett PH (1998) Intrauterine diabetes exposure and the risk of renal disease in diabetic Pima Indians. Diabetes 47:1489–1493CrossRefPubMed

24.

Aceti A, Santhakumaran S, Logan KM et al (2012) The diabetic pregnancy and offspring blood pressure in childhood: A systematic review and meta-analysis. Diabetologia 55:3114–3127CrossRefPubMed

25.

Azad MB, Becker AB, Kozyrskyj AL (2013) Association of maternal diabetes and child asthma. Pediatr Pulmonol 48:545–552CrossRefPubMed

26.

Pirkola J, Vaarasmaki M, Leinonen E et al (2008) Maternal type 1 and gestational diabetes: Postnatal differences in insulin secretion in offspring at preschool age. Pediatr Diabetes 9:583–589CrossRefPubMed

27.

Abi Khalil C, Travert F, Fetita S et al (2010) Fetal exposure to maternal type 1 diabetes is associated with renal dysfunction at adult age. Diabetes 59:2631–2636CrossRefPubMed

28.

Perna R, Loughan AR, Le J et al (2015) Gestational diabetes: Long-term central nervous system developmental and cognitive sequelae. Appl Neuropsychol Child 4:217–220CrossRefPubMed

29.

Camprubi Robles M, Campoy C, Garcia Fernandez L et al (2015) Maternal diabetes and cognitive performance in the offspring: A systematic review and meta-analysis. PLoS ONE 10:e0142583CrossRefPubMedPubMedCentral

30.

Philipps LH, Santhakumaran S, Gale C et al (2011) The diabetic pregnancy and offspring BMI in childhood: A systematic review and meta-analysis. Diabetologia 54:1957–1966CrossRefPubMed

31.

Rocha SO, Gomes GN, Forti AL et al (2005) Long-term effects of maternal diabetes on vascular reactivity and renal function in rat male offspring. Pediatr Res 58:1274–1279CrossRefPubMed

32.

Yan J, Li X, Su R et al (2014) Long-term effects of maternal diabetes on blood pressure and renal function in rat male offspring. PLoS ONE 9:e88269CrossRefPubMedPubMedCentral

33.

Nehiri T, Duong Van Huyen JP, Viltard M et al (2008) Exposure to maternal diabetes induces salt-sensitive hypertension and impairs renal function in adult rat offspring. Diabetes 57:2167–2175CrossRefPubMedPubMedCentral

34.

Franke K, Harder T, Aerts L et al (2005) ‚Programming‘ of orexigenic and anorexigenic hypothalamic neurons in offspring of treated and untreated diabetic mother rats. Brain Res 1031:276–283CrossRefPubMed

35.

Ma RC, Tutino GE, Lillycrop KA et al (2015) Maternal diabetes, gestational diabetes and the role of epigenetics in their long term effects on offspring. Prog Biophys Mol Biol 118:55–68CrossRefPubMed

36.

Dunn GA, Bale TL (2009) Maternal high-fat diet promotes body length increases and insulin insensitivity in second-generation mice. Endocrinology 150:4999–5009CrossRefPubMedPubMedCentral

37.

Remely M, De La Garza AL, Magnet U et al (2015) Obesity: Epigenetic regulation – recent observations. Biomol Concepts 6:163–175CrossRefPubMed

38.

Vickers MH (2014) Developmental programming and transgenerational transmission of obesity. Ann Nutr Metab 64(Suppl 1):26–34CrossRefPubMed

39.

Dunn GA, Bale TL (2011) Maternal high-fat diet effects on third-generation female body size via the paternal lineage. Endocrinology 152:2228–2236CrossRefPubMedPubMedCentral

40.

Hanafi MY, Abdelkhalek TM, Saad MI et al (2016) Diabetes-induced perturbations are subject to intergenerational transmission through maternal line. J Physiol Biochem 72:315–326CrossRefPubMed

41.

Ponzio BF, Carvalho MH, Fortes ZB et al (2012) Implications of maternal nutrient restriction in transgenerational programming of hypertension and endothelial dysfunction across F1–F3 offspring. Life Sci 90:571–577CrossRefPubMed

42.

Hogg K, Price EM, Hanna CW et al (2012) Prenatal and perinatal environmental influences on the human fetal and placental epigenome. Clin Pharmacol Ther 92:716–726CrossRefPubMed

43.

Tobi EW, Lumey LH, Talens RP et al (2009) DNA methylation differences after exposure to prenatal famine are common and timing- and sex-specific. Hum Mol Genet 18:4046–4053CrossRefPubMedPubMedCentral

44.

Tobi EW, Slagboom PE, Van Dongen J et al (2012) Prenatal famine and genetic variation are independently and additively associated with DNA methylation at regulatory loci within IGF2/H19. PLoS ONE 7:e37933CrossRefPubMedPubMedCentral

45.

Godfrey KM, Sheppard A, Gluckman PD et al (2011) Epigenetic gene promoter methylation at birth is associated with child’s later adiposity. Diabetes 60:1528–1534CrossRefPubMedPubMedCentral

46.

Alejandro EU, Gregg B, Wallen T et al (2014) Maternal diet-induced microRNAs and mTOR underlie beta cell dysfunction in offspring. J Clin Invest 124:4395–4410CrossRefPubMedPubMedCentral

47.

Dotsch J, Plank C, Amann K (2012) Fetal programming of renal function. Pediatr Nephrol 27:513–520CrossRefPubMed

48.

Keller G, Zimmer G, Mall G et al (2003) Nephron number in patients with primary hypertension. N Engl J Med 348:101–108CrossRefPubMed

49.

Rother E, Kuschewski R, Alcazar MA et al (2012) Hypothalamic JNK1 and IKKbeta activation and impaired early postnatal glucose metabolism after maternal perinatal high-fat feeding. Endocrinology 153:770–781CrossRefPubMed

50.

Vogt MC, Paeger L, Hess S et al (2014) Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding. Cell 156:495–509CrossRefPubMedPubMedCentral

51.

Nusken KD, Schneider H, Plank C et al (2011) Fetal programming of gene expression in growth-restricted rats depends on the cause of low birth weight. Endocrinology 152:1327–1335CrossRefPubMed

52.

Bouchard L (2013) Epigenetics and fetal metabolic programming: A call for integrated research on larger cohorts. Diabetes 62:1026–1028CrossRefPubMedPubMedCentral

53.

Rabadan-Diehl C, Nathanielsz P (2013) From Mice to Men: Research models of developmental programming. J Dev Orig Health Dis 4:3–9CrossRefPubMedPubMedCentral

Titel: Perinatale Programmierung des Typ-2-Diabetes
verfasst von: R. Ensenauer
E. Hucklenbruch-Rother
V. Brüll
Prof. Dr. J. Dötsch
Publikationsdatum: 07.09.2016
Verlag: Springer Berlin Heidelberg
Schlagwörter: Typ-2-Diabetes
Intrauterine Wachstumsrestriktion
Diabetes mellitus
Adipositas
Adipositas
Gestationsdiabetes
Gestationsdiabetes
Epigenetik
Erschienen in: Die Diabetologie / Ausgabe 6/2016
Print ISSN: 2731-7447
Elektronische ISSN: 2731-7455
DOI: https://doi.org/10.1007/s11428-016-0126-1

Praxisempfehlungen der Deutschen Diabetes Gesellschaft

Kurz, prägnant und aktuell: Die Praxisempfehlungen der Deutschen Diabetes Gesellschaft.

Zu den Praxisempfehlungen

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Springer Medizin

Perinatale Programmierung des Typ-2-Diabetes

Zusammenfassung

Praxisempfehlungen der Deutschen Diabetes Gesellschaft

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Springer Medizin

Zusammenfassung

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 6/2016

Fäkale Mikrobiotatransplantation

Magazin

Wirkungsmechanismus von Canagliflozin

Mitteilungen des BDE

Wie die Ernährung das Mikrobiom beeinflusst

Auswirkungen von Liraglutid auf die Hirnaktivität

Praxisempfehlungen der Deutschen Diabetes Gesellschaft