Glucose metabolism in pregnancy and embryogenesis

Current Opinion in Endocrinology, Diabetes and Obesity

Volumn 14, Issue 6, 2007, Pages 488-493

  Doblado, Manuel ^a   Moley, Kelle H ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Glucose metabolism; Glucose transport; Maternal diabetes; Maternal hyperglycemia

Indexed keywords

GLUCOSE; GLUCOSE TRANSPORTER;

ARTICLE; DIABETES MELLITUS; EMBRYO DEVELOPMENT; GLUCOSE HOMEOSTASIS; GLUCOSE METABOLISM; GLUCOSE TRANSPORT; HUMAN; HYPERGLYCEMIA; NONHUMAN; OOCYTE DEVELOPMENT; PREGNANCY; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION;

ANIMALS; EMBRYO, MAMMALIAN; EMBRYONIC DEVELOPMENT; FEMALE; GLUCOSE; GLUCOSE TRANSPORT PROTEINS, FACILITATIVE; HOMEOSTASIS; HUMANS; OOCYTES; PREGNANCY; PREGNANCY IN DIABETICS;

EID: 35848934548     PISSN: 1752296X     EISSN: None     Source Type: Journal    
DOI: 10.1097/MED.0b013e3282f1cb92     Document Type: Article

References (58)

1. Casson IF, Clarke CA, Howard CV, et al. Outcomes of pregnancy in insulin dependent diabetic women: results of a five year population cohort study. BMJ 1997; 315:275-278.
2. Baccetti B, La Marca A, Piomboni P, et al. Insulin-dependent diabetes in men is associated with hypothalamo-pituitary derangement and with impairment in semen quality. Hum Reprod 2002; 17:2673-2677.
3. Reece EA, Eriksson UJ. The pathogenesis of diabetes-associated congenital malformations. Obstet Gynecol Clin North Am 1996; 23:29-45.
4. Ivanisevic M, Bukovic D, Starcevic V, et al. Influence of hyperglycemia on early embryonal growth in IDDM pregnant women. Coll Antropol 1999; 23:183-188.
5. El-Sayed Y, Lyell D. New therapies for the pregnant patient with diabetes. Diabetes Technol Therapeut 2001; 3:635-640.
6. Greene MF. Spontaneous abortions and major malformations in women with diabetes mellitus. Semin Reprod Endocrinol 1999; 17:127-136.
7. Moley KH, Chi MM-Y, Mueckler M. Maternal hyperglycemia alters glucose transport and utilization in mouse preimplantation embryos. Am J Physiol Endocrinol Metab 1998; 275:E38-E47.
8. Moley KH, Chi MM-Y, Knudson CM, et al. Hyperglycemia induces apoptosis in preimplantation embryos via cell death effector pathways. Nat Med 1998; 12:1421-1424.
9. Diamond MP, Moley KH, Pellicer A, et al. Effects of streptozotocin- and alloxan-induced diabetes mellitus on mouse follicular and early embryo development. J Reprod Fertil 1989; 86:1-10.
10. Chi MM, Pingsterhaus J, Carayannopoulos M, Moley KH. Decreased glucose transporter expression triggers BAX-dependent apoptosis in the murine blastocyst. J Biol Chem 2000; 275:40252-40257.
11. Moley KH, Vaughn WK, DeCherney AH, Diamond MP. Effect of diabetes mellitus on mouse preimplantation embryo development. J Reprod Fertil 1991; 93:325-332.
12. Kwong WY, Wild AE, Roberts P, et al. Maternal undernutrition during the preimplantation period of rat development causes blastocyst abnormalities and programming of postnatal hypertension. Development 2000; 127:4195-4202.
13. Fleming JV, Hay SM, Harries DN, Rees WD. Effects of nutrient deprivation and differentiation on the expression of growth-arrest genes (gas and gadd) in F9 embryonal carcinoma cells. Biochem J 1998; 330:573-579.
14. Fleming JV, Fontanier N, Harries DN, Rees WD. The growth arrest genes gas5, gas6, and CHOP-10 (gadd153) are expressed in the mouse preimplantation embryo. Mol Reprod Dev 1997; 48:310-316.
15. Lane M, Gardner DK. Differential regulation of mouse embryo development and viability by amino acids. J Reprod Fertil 1997; 109:153-164.
16. Johansson S, Norman M, Legnevall L, et al. Increased catecholamines and heart rate in children with low birth weight: perinatal contributions to sympathoadrenal overactivity. J Intern Med 2007; 261:480-487.
17. Johansson S, Iliadou A, Bergvall N, et al. Risk of high blood pressure among young men increases with the degree of immaturity at birth. Circulation 2005; 112:3430-3436.
18. Gardner DK, Lane M. Amino acids and ammonium regulate mouse embryo development in culture. Biol Reprod 1993; 48:377-385.
19. Van Assche FA, Holemans K, Aerts L. Long-term consequences for offspring of diabetes during pregnancy. Br Med Bull 2001; 60:173-182.
20. Dabelea D, Pettitt DJ. Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. J Pediatr Endocrinol Metab 2001; 14:1085-1091.
21. Garris DR, Williams SK, West L. Morphometric evaluation of diabetes-associated ovarian atrophy in the C57BL/KsJ mouse: relationship to age and ovarian function. Anat Rec 1985; 211:434-443.
22. Colton SA, Humpherson PG, Leese HJ, Downs SM. Physiological changes in oocyte-cumulus cell complexes from diabetic mice that potentially influence meiotic regulation. Biol Reprod 2003; 69:761-770.
23. Kim K, Kim C, Moley K, Cheon Y-P. Disordered meiotic regulation of oocytes by duration of diabetes mellitus in BBdp rat. Reprod Sci 2007 (in press).
24. Chang AS, Dale AN, Moley KH. Maternal diabetes adversely affects preovulatory oocyte maturation, development, and granulosa cell apoptosis. Endocrinology 2005; 146:2445-2453.
25. Idil M, Cepni I, Demirsoy G, et al. Does granulosa cell apoptosis have a role in the etiology of unexplained infertility? Eur J Obstet Gynecol Reprod Biol 2004; 112:182-184.
26. Lee KS, Joo BS, Na YJ, et al. Cumulus cells apoptosis as an indicator to predict the quality of oocytes and the outcome of IVF-ET. J Assist Reprod Genet 2001; 18:490-498.
27. Nakahara K, Saito H, Saito T, et al. The incidence of apoptotic bodies in membrana granulosa can predict prognosis of ova from patients participating in in vitro fertilization programs. Fertil Steril 1997; 68:312-317.
28. Ackert CL, Gittens JE, O'Brien MJ, et al. Intercellular communication via connexin43 gap junctions is required for ovarian folliculogenesis in the mouse. Dev Biol 2001; 233:258-270.
29. Atef A, Francois P, Christian V, Marc-Andre S. The potential role of gap junction communication between cumulus cells and bovine oocytes during in vitro maturation. Mol Reprod Dev 2005; 71:358-367.
30. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature 2001; 414:813-820.
31. Nishikawa T, Edelstein D, Du XL, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature 2000; 404:787-790.
32. Du XL, Edelstein D, Dimmeler S, et al. Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site. J Clin Invest 2001; 108:1341-1348.
33. Khorram O. Nitric oxide and its role in blastocyst implantation. Rev Endocr Metab Disord 2002; 3:145-149.
34. Nishikimi A, Matsukawa T, Hoshino K, et al. Localization of nitric oxide synthase activity in unfertilized oocytes and fertilized embryos during preimplantation development in mice. Reproduction 2001; 122:957-963.
35. Moncada S, Palmer RM, Higgs EA. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev 1991; 43:109-142.
36. Goud PT, Goud AP, Leybaert L, et al. Inositol 1,4,5-trisphosphate receptor function in human oocytes: calcium responses and oocyte activation-related phenomena induced by photolytic release of InsP(3) are blocked by a specific antibody to the type I receptor. Mol Hum Reprod 2002; 8:912-918.
37. Goud AP, Goud PT, Diamond MP, et al. Activation of the cGMP signaling pathway is essential in delaying oocyte aging in diabetes mellitus. Biochemistry 2006; 45:11366-11378. This paper presents the results of experiments that suggest the importance of the nitric oxide signaling pathway in oocyte aging.
38. Ratchford AM, Chang AS, Chi MM, et al. Maternal diabetes adversely affects AMP-activated protein kinase activity and cellular metabolism in murine oocytes. Am J Physiol Endocrinol Metab 2007 (in press).
39. Thatcher SS, Jackson EM. Pregnancy outcome in infertile patients with polycystic ovary syndrome who were treated with metformin. Fertil Steril 2006; 85:1002-1009.
40. Vanky E, Salvesen KA, Heimstad R, et al. Metformin reduces pregnancy complications without affecting androgen levels in pregnant polycystic ovary syndrome women: results of a randomized study. Hum Reprod 2004; 19:1734-1740.
41. Simmons D, Walters BN, Rowan JA, McIntyre HD. Metformin therapy and diabetes in pregnancy. Med J Aust 2004; 180:462-464.
42. Glueck CJ, Goldenberg N, Wang P, et al. Metformin during pregnancy reduces insulin, insulin resistance, insulin secretion, weight, testosterone and development of gestational diabetes: prospective longitudinal assessment of women with polycystic ovary syndrome from preconception throughout pregnancy. Hum Reprod 2004; 19:510-521.
43. Moley KH, Vaughn WK, Diamond MP. Manifestations of diabetes mellitus on mouse preimplantation development: effect of elevated concentration of metabolic intermediates. Hum Reprod 1994; 9:113-121.
44. Riley JK, Carayannopoulos MO, Wyman AH, et al. The PI3K/Akt pathway is present and functional in the preimplantation mouse embryo. Dev Biol 2005; 284:377-386.
45. Leese HJ. Energy metabolism of the preimplantation embryo. In: Wiley LM, Heyner S, editors. Early embryo development and paracrine relationships. UCLA Symposia on Molecular and Cellular Biology. New York: Wiley-Liss; 1991. pp. 67-78.
46. Pinto A, Carayannopoulos M, Hoehn A, et al. GLUT8 expression and translocation are critical for murine blastocyst survival. Biol Reprod 2002; 66:1729-1733.
47. Carayannopoulos MO, Chi MM, Cui Y, et al. GLUT8 is a glucose transporter responsible for insulin-stimulated glucose uptake in the blastocyst. Proc Natl Acad Sci USA 2000; 97:7313-7318.
48. Heilig CW, Saunders T, Brosius FC 3rd, et al. Glucose transporter-1-deficient mice exhibit impaired development and deformities that are similar to diabetic embryopathy. Proc Natl Acad Sci USA 2003; 100:15613-15618.
49. Mills JL. Malformations in infants of diabetic mothers. Teratology 1982; 25:385-394.
50. Lindstrom JA. A diabetic embryopathy: the caudal regression syndrome. Birth Defects Orig Artic Ser 1971; 7:278-279.
51. Pantaleon M, Harvey MB, Pascoe WS, et al. Glucose transporter GLUT3: Ontogeny, targeting and role in the mouse blastocyst. Proc Natl Acad Sci USA 1997; 94:3795-3800.
52. Ganguly A, McKnight RA, Raychaudhuri S, et al. Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction. Am J Physiol Endocrinol Metab 2007; 292:E1241-E1255. This paper reports the results of several experiments that show the importance of GLUT3 in early pregnancy and fetal development.
53. Lea RG, McCracken JE, McIntyre SS, et al. Disturbed development of the preimplantation embryo in the insulin-dependent diabetic BB/E rat. Diabetes 1996; 45:1463-1470.
54. Pampfer S, Vanderheyden I, McCracken JE, et al. Increased cell death in rat blastocysts exposed to maternal diabetes in utero and to high glucose or tumor necrosis factor-alpha in vitro. Development 1997; 124:4827-4836.
55. Franke TF, Kaplan DR, Cantley LC. PI3K: downstream AKTion blocks apoptosis. Cell 1997; 88:435-437.
56. Franke TF, Cantley LC. Apoptosis. a Bad kinase makes good. Nature 1997; 390:116-117.
57. Eng GS, Sheridan RA, Wyman A, et al. AMPK activation increases glucose uptake, decreases apoptosis and improves pregnancy outcome in embryos exposed to high IGF-1 concentrations. Diabetes 2007; 56:2228-2234. This study suggests that hyperinsulinemia results in decreased AMPK activation and that metformin, an activator of AMPK, can prevent the effects of hyperinsulinemia on early blastocysts.
58. Riley JK, Carayannopoulos MO, Wyman AH, et al. Phosphatidylinositol 3-kinase activity is critical for glucose metabolism and embryo survival in murine blastocysts. J Biol Chem 2006; 281:6010-6019. This paper reports on experiments showing the importance of the PI3K signal transduction pathway in the regulation of glucose transport and embryo development.