#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Birth weight and genetic risk of type 2 diabetes in Czech population


Authors: D. Vejražková;  M. Vaňková;  P. Lukášová;  J. Včelák;  O. Bradnová;  S. Pražáková;  H. Kvasničková;  B. Bendlová
Authors place of work: Oddělení molekulární endokrinologie Endokrinologického ústavu Praha, ředitel doc. MU Dr. Vojtěch Hainer, CSc.
Published in the journal: Vnitř Lék 2010; 56(12): 1303-1309
Category: Celebration

Summary

Introduction:
Birth weight is associated with type 2 diabetes mellitus and other late‑ onset metabolic diseases. Reduced birth weight is associated with an increased risk of insulin resistance, type 2 diabetes, and atherosclerosis. Also high birth weight represents risk factor for development of type 2 diabetes later in life. In this study, we investigate whether type 2 diabetes risk‑confering alleles and bio­chemical as well as anthropometrical type 2 diabetes risk markers associate with birth weight in our Czech cohort.

Results:
Association between high birth weight and higher BMI in adulthood was found. Low birth weight was associated with higher glycaemia and insulinaemia as well as lower peripheral insulin sensitivity during oGTT. The examination of candidate genes provides evidence that Ngn3 and PPARα are involved in final birth weight regulation.

Conclusion:
According to our results, we suggest that birth weight should be an integral part of medical history record.

Key words:
birth weight –  type 2 diabetes mellitus –  body composition –  insulin sensitivity –  type 2 diabetes mellitus candidate genes


Zdroje

1. Barker DJ, Hales CN, Fall CH et al. Type 2 (non‑insulin‑dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia 1993; 36: 62– 67.

2. Hales CN, Barker DJ, Clark PM et al. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ 1991; 303: 1019– 1022.

3. Frayling TM, Hattersley AT. The role of genetic susceptibility in the association of low birth weight with type 2 diabetes. Br Med Bull 2001; 60: 89– 101.

4. Harder T, Rodekamp E, Schellong K et al. Birth weight and subsequent risk of type 2 diabetes: a meta‑analysis. Am J Epidemiol 2007; 165: 849– 857.

5. Whincup PH, Kaye SJ, Owen CG et al. Birth weight and risk of type 2 diabetes: a systematic review. JAMA 2008; 300: 2886– 2897.

6. Godfrey KM, Barker DJ. Fetal nutrition and adult disease. Am J Clin Nutr 2000; 71 (Suppl 5): 1344S– 1352S.

7. Meas T, Deghmoun S, Alberti C et al. Independent effects of weight gain and fetal programming on metabolic complications in adults born small for gestational age. Diabetologia 2010; 53: 907– 913.

8. Hattersley AT, Beards F, Ballantyne E et al. Mutations in the glucokinase gene of the fetus result in reduced birth weight. Nat Genet 1998; 19: 268– 270.

9. Hattersley AT, Tooke JE. The fetal insulin hypothesis: an alternative explanation of the association of low birthweight with diabetes and vascular disease. Lancet 1999; 353: 1789– 1792.

10. Ong KK, Dunger DB. Thrifty genotypes and phenotypes in the pathogenesis of type 2 diabetes mellitus. J Pediatr Endocrinol Metab 2000; 13 (Suppl 6): 1419– 1424.

11. Ong KK, Ahmed ML, Emmett PM et al. Association between postnatal catch‑ up growth and obesity in childhood: prospective cohort study. BMJ 2000; 320: 967– 971.

12. Stettler N, Bovet P, Shamlaye H et al. Prevalence and risk factors for overweight and obesity in children from Seychelles, a country in rapid transition: the importance of early growth. Int J Obes Relat Metab Disord 2002; 26: 214– 219.

13. Stettler N, Zemel BS, Kumanyika S et al. Infant weight gain and childhood overweight status in a multicenter, cohort study. Pediatrics 2002; 109: 194– 199.

14. Yajnik C. Interactions of perturbations in intrauterine growth and growth during childhood on the risk of adult‑ onset disease. Proc Nutr Soc 2000; 59: 257– 265.

15. Durmuş B, Mook‑ Kanamori DO, Holzhauer S et al. Growth in foetal life and infancy is associated with abdominal adiposity at the age of 2 years: the generation R study. Clin Endocrinol (Oxf) 2010; 72: 633– 640.

16. Ibáñez L, Ong K, de Zegher F et al. Fat distribution in non‑obese girls with and without precocious pubarche: central adiposity related to insulinaemia and androgenaemia from prepuberty to postmenarche. Clin Endocrinol (Oxf) 2003; 58: 372– 379.

17. Tzoulaki I, Sovio U, Pillas D et al. Relation of immediate postnatal growth with obesity and related metabolic risk factors in adulthood: the northern Finland birth cohort 1966 study. Am J Epidemiol 2010; 171: 989– 998.

18. Slingerland AS, Hattersley AT. Activating mutations in the gene encoding Kir6.2 alter fetal and postnatal growth and also cause neonatal diabetes. J Clin Endocrinol Metab 2006; 91: 2782– 2788.

19. Støy J, Edghill EL, Flanagan SE et al. Insulin gene mutations as a cause of permanent neonatal diabetes. Proc Natl Acad Sci USA 2007; 104: 15040– 15044.

20. Babenko AP, Polak M, Cavé H et al. Activating mutations in the ABCC8 gene in neonatal diabetes mellitus. N Engl J Med 2006; 355: 456– 466.

21. Edghill EL, Bingham C, Slingerland AS et al. Hepatocyte nuclear factor‑ 1 beta mutations cause neonatal diabetes and intrauterine growth retardation: support for a critical role of HNF‑ 1beta in human pancreatic development. Diabet Med 2006; 23: 1301– 1306.

22. Freathy RM, Bennett AJ, Ring SM et al. Type 2 diabetes risk alleles are associated with reduced size at birth. Diabetes 2009; 58: 1428– 1433.

23. Zhao J, Li M, Bradfield JP et al. Examination of type 2 diabetes loci implicates CDKAL1 as a birth weight gene. Diabetes 2009; 58: 2414– 2418.

24. Eriksson JG, Forsen TJ, Osmond C et al. Pathways of infant and childhood growth that lead to type 2 diabetes. Diabetes Care 2003; 26: 3006– 3010.

25. Pulizzi N, Lyssenko V, Jonsson A et al. Interaction between prenatal growth and high‑risk genotypes in the development of type 2 diabetes. Diabetologia 2009; 52: 825– 829.

26. Dabelea D, Hanson RL, Lindsay RS et al. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes 2000; 49: 2208– 2211.

27. Martin R, Saller K. Lehrbuch der Anthropologie in systematischer Darstellung. Stuttgart: G. Fischer Verlag 1959.

28. Bláha P. Antropo –  ein Programm für automatische Bearbeitung antropologischer Daten. Wiss. Zeitschrift der Humboldt‑ Universitat zu Berlin 1991; 5: 153– 156.

29. Cederholm J, Wibell L. Insulin release and peripheral sensitivity at the oral glucose tolerance test. Diabetes Res Clin Pract 1990; 10: 167– 175.

30. Radikova Z. Assessment of insulin sensitivity/ resistance in epidemiological studies. Endocr Regul 2003; 37: 189– 194.

31. Wang J, Cortina G, Wu SV et al. Mutant neurogenin‑3 in congenital malabsorptive diarrhea. N Engl J Med 2006; 355: 270– 280.

32. Edghill EL, Minton JA, Groves CJ et al. Sequencing of candidate genes selected by beta cell experts in monogenic diabetes of unknown aetiology. JOP 2010; 11: 14– 17.

33. Jiang FX, Mehta M, Morahan G. Quantification of insulin gene expression during development of pancreatic islet cells. Pancreas 2010; 39: 201– 208.

34. Danilova OV, Tai AK, Mele DA et al. Neurogenin 3- specific dipeptidyl peptidase‑ 2 deficiency causes impaired glucose tolerance, insulin resistance, and visceral obesity. Endocrinology 2009; 150: 5240– 5248.

35. Yechoor V, Liu V, Paul A et al. Gene therapy with neurogenin 3 and betacellulin reverses major metabolic problems in insulin‑deficient diabetic mice. Endocrinology 2009; 150: 4863– 4873.

36. Silbernagel G, Stefan N, Hoffmann MM et al. The L162V polymorphism of the peroxisome proliferator activated receptor alpha gene (PPARA) is not associated with type 2 diabetes, BMI or body fat composition. Exp Clin Endocrinol Diabetes 2009; 117: 113– 118.

37. Ordovas JM. Genetic links between diabetes mellitus and coronary atherosclerosis. Curr Atheroscler Rep 2007; 9: 204– 210.

38. Andrulionyte L, Kuulasmaa T, Chiasson JL et al. Single nucleotide polymorphisms of the peroxisome proliferator‑activated receptor‑alpha gene (PPARA) influence the conversion from impaired glucose tolerance to type 2 diabetes: the STOP‑ NIDDM trial. Diabetes 2007; 56: 1181– 1186.

39. Williams PJ, Marten N, Wilson V et al. Influence of birth weight on gene regulators of lipid metabolism and utilization in subcutaneous adipose tissue and skeletal muscle of neonatal pigs. Reproduction 2009; 138: 609– 617.

Štítky
Diabetology Endocrinology Internal medicine

Článok vyšiel v časopise

Internal Medicine

Číslo 12

2010 Číslo 12
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#