妊娠期糖尿病的遗传学研究进展(2)
综上所述，现今发现的与GDM发病相关联的基因越来越多，他们或者影响了胰岛素发挥作用的正常途径，或者影响了β细胞的正常代谢和信号通路，或者通过基因多态性使GDM具有一定的易感性等，引起了机体代谢的紊乱，诱发了GDM的产生。虽然很多研究表明了这些基因和GDM有相关性，但由于样本基数还太少，有必要在不同种群更大的范围内做相关性分析，从而更好地深入料及GDM发病的遗传学原因。
参考文献：
[1] Phillips, P.J. and B. Jeffries, Gestational diabetes--worth finding and actively treating. Aust Fam Physician, 2006. 35(9): p. 701-3.
[2] Bennett, S.T. and J.A. Todd, Human type 1 diabetes and the insulin gene: principles of mapping polygenes. Annu Rev Genet, 1996. 30: p. 343-70.
[3] McGettrick, A.J., E.P. Feener, and C.R. Kahn, Human insulin receptor substrate-1 (IRS-1) polymorphism G972R causes IRS-1 to associate with the insulin receptor and inhibit receptor autophosphorylation. J Biol Chem, 2005. 280(8): p. 6441-6.
[4] Fallucca, F., et al., Polymorphisms of insulin receptor substrate 1 and beta3-adrenergic receptor genes in gestational diabetes and normal pregnancy. Metabolism, 2006. 55(11): p. 1451-6.
[5] Denley, A., et al., Molecular interactions of the IGF system. Cytokine Growth Factor Rev, 2005. 16(4-5): p. 421-39.
[6] Gloyn, A.L., J. Siddiqui, and S. Ellard, Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat, 2006. 27(3): p. 220-31.
[7] Vaxillaire, M. and P. Froguel, Genetic basis of maturity-onset diabetes of the young. Endocrinol Metab Clin North Am, 2006. 35(2): p. 371-84, x.
[8] Shaat, N., et al., Common variants in MODY genes increase the risk of gestational diabetes mellitus. Diabetologia, 2006. 49(7): p. 1545-51., 百拇医药(林丽苹)
参考文献：
[1] Phillips, P.J. and B. Jeffries, Gestational diabetes--worth finding and actively treating. Aust Fam Physician, 2006. 35(9): p. 701-3.
[2] Bennett, S.T. and J.A. Todd, Human type 1 diabetes and the insulin gene: principles of mapping polygenes. Annu Rev Genet, 1996. 30: p. 343-70.
[3] McGettrick, A.J., E.P. Feener, and C.R. Kahn, Human insulin receptor substrate-1 (IRS-1) polymorphism G972R causes IRS-1 to associate with the insulin receptor and inhibit receptor autophosphorylation. J Biol Chem, 2005. 280(8): p. 6441-6.
[4] Fallucca, F., et al., Polymorphisms of insulin receptor substrate 1 and beta3-adrenergic receptor genes in gestational diabetes and normal pregnancy. Metabolism, 2006. 55(11): p. 1451-6.
[5] Denley, A., et al., Molecular interactions of the IGF system. Cytokine Growth Factor Rev, 2005. 16(4-5): p. 421-39.
[6] Gloyn, A.L., J. Siddiqui, and S. Ellard, Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat, 2006. 27(3): p. 220-31.
[7] Vaxillaire, M. and P. Froguel, Genetic basis of maturity-onset diabetes of the young. Endocrinol Metab Clin North Am, 2006. 35(2): p. 371-84, x.
[8] Shaat, N., et al., Common variants in MODY genes increase the risk of gestational diabetes mellitus. Diabetologia, 2006. 49(7): p. 1545-51., 百拇医药(林丽苹)