2005, Número 07
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Ginecol Obstet Mex 2005; 73 (07)
Conceptos recientes en la etiopatogenia de la diabetes gestacional
Hernández VM, Zárate A
Idioma: Español
Referencias bibliográficas: 36
Paginas: 371-377
Archivo PDF: 63.18 Kb.
RESUMEN
Los cambios en la acción de la insulina condicionan la adaptación del metabolismo materno para favorecer la disposición de los nutrientes que requiere el feto en su desarrollo; de esta forma se establece un estado de resistencia a la insulina que genera mayor producción de insulina a fin de compensar dicha resistencia. Sin embargo, las células-β del páncreas podrían estar lesionadas y ser insuficientes para compensar esta demanda. Las causas a las que se atribuye el desencadenamiento de la diabetes gestacional son: concentración elevada de las hormonas placentarias; péptidos producidos por el tejido adiposo, a los cuales se les ha asignado un factor de predicción para el desencadenamiento de resistencia a la insulina; efecto adverso de la mala nutrición en la vida intrauterina; autoinmunidad que se activa por el consumo de algunos nutrientes en la vida neonatal; procesos virales que aparecen en la niñez. Esto puede lesionar los islotes pancreáticos y volverlos deficientes para reaccionar a una sobrecarga metabólica como el embarazo.
REFERENCIAS (EN ESTE ARTÍCULO)
Casey BM, Lucas MJ, McIntire DD, Leveno KJ. Pregnancy outcomes in women with gestational diabetes compared with the general obstetric population. Obstet Gynecol 1997;90:869-73.
Sermer M, Naylor CD, Gare DJ, et al. Impact of increasing carbohydrate intolerance on maternal-fetal outcomes in 3637 women without gestational diabetes. The Toronto Tri-Hospital Gestational Diabetes Project. Am J Obstet Gynecol 1995;173:146-56.
Hernández-Valencia M, Carrillo PA. Control prenatal asociado al número de consultas como método diagnóstico de hiperglucemia. Ginecol Obst Mex 2002;70:592-6.
Metzger BE, Phelps RL, Freinkel N, Navickas IA. Effects of gestational diabetes on diurnal profiles of plasma glucose, lipids, and individual amino acids. Diabetes Care 1980;3:402-9.
Catalo PM, Drago NM, Amini SB. Maternal carbohydrate metabolism and its relationship to fetal growth and body composition. Am J Obstet Gynecol 1995;172:1464-70.
Hernández-Valencia M, Zárate A. El riesgo de diabetes gestacional se establece desde la vida fetal y postnatal. Ginecol Obst Mex 2003;71:60-65.
Wood SL, Sauve R, Ross S, et al. Prediabetes and perinatal mortality. Diabetes Care 2000;23:1752-4.
Kuhl C. Insulin secretion and insulin resistance in pregnancy and GDM. Implications for diagnosis and management. Diabetes 1991;40 (Suppl 2):18-24.
Ryan EA. Hormones and insulin resistance during pregnancy. Lancet 2003;362:1-3.
Buchanan TA, Metzger BE, Freinkel N, Bergman RN. Insulin sensitivity and beta-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes. Am J Obstet Gynecol 1990;162:1008-14.
Catalano PM, Tyzibir ED, Roman NM, et al. Longitudinal changes in insulin resistance in non-obese pregnant women. Am J Obstet Gynecol 1991;165:1667-772.
Sivan E, Chen X, Homko CJ, et al. Longitudinal study of carbohydrate metabolism in healthy obese pregnant women. Diabetes Care 1997;20:1470-5.
Sugden MC, Greenwood GK, Smith ND, Holness MJ. Peroxisome proliferators-activated receptor-a activation during pregnancy attenuates glucose-stimulated insulin hypersecretion in vivo by increasing insulin sensitivity, without impairing pregnancy-induced increases in b-cell glucose sensing and responsiveness. Endocrinology 2003;144:146-53.
Melczer Z, Bánhidy F, Csomor S. Influence of leptin and the TNF system on insulin resistance in pregnancy and their effect on anthropometric parameters of newborns. Acta Obstet Gynecol Scand 2003;82:432-8.
Winzer C, Wagner O, Festa A, et al. Plasma adiponectin, insulin sensitivity, and subclinical inflammation in women with prior gestational diabetes mellitus. Diabetes Care 2004;27:1721-7.
Steppan CM, Bailey ST, Bhat S. The hormone resistin links obesity to diabetes. Nature 2001;409:307-12.
Catalano PM, Nizielski SE, Shao J, et al. Down regulated IRS-1 and PPAR-g in obese women with gestational diabetes: relationship to FFA during pregnancy. Am J Physiol Endocrinol Metab 2002;282:522-33.
Kirwan JP, Hauguel-De Mouzon S, et al. TNF-a is a predictor of insulin resistance in human pregnancy. Diabetes 2002;51:2207-13.
Ziegler AG, Hummel M, Schenker M, Bonifacio E. Autoantibody appearance and risk for the development of childhood diabetes in offspring of parents with type 1 diabetes: the German BABY-DIAB study. Diabetes 1999;48:460-8.
Ziegler AG, Schmid A, Huber D, et al. Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies. JAMA 2003;290:1721-8.
Hyoty H, Taylor KW. The role of viruses in human diabetes. Diabetologia 2002;45:1353-61.
Moriyama H, Wen L, Abiru N, et al. Induction and acceleration of insulin/diabetes in mice with a viral mimic (polyinosinic-polycytidylic acid) and an insulin self-peptide. Proc Natl Acad Sci USA 2002;99:5539-44.
Friedman JE, Ishizuka T, Huston L, et al. Impaired glucose transport and insulin receptor tyrosine phosphorylation in obese women with gestational diabetes mellitus. Diabetes 1999;48:1807-14.
Puavilai G, Dorbny EC, Domont LA. Insulin receptors and insulin resistance in human pregnancy: evidence for a postreceptor defect in insulin action. J Clin Endocrinol Metab 1982;54:247-53.
Damm P, Handberg A, Kuhl C, et al. Insulin receptor binding and tyrosine kinase in skeletal muscle from normal pregnant women and women with gestational diabetes. Obstet Gynecol 1993;82:251-9.
White MF, Shoelson SE, Keutmann H, Kahn CR. A cascade of tyrosine autophosphorylation in the b-subunit activates the insulin receptor. J Biol Chem 1988;263:2969-75.
Wilden PA, Siddel K, Haring H, et al. The role of insulin receptor kinase domain autophosphorylation in receptor-mediated activities. J Biol Chem 1992;267:13719-26.
White MF, Kahn CR. The insulin signaling system. J Biol Chem 1994;269:1-4.
Nolan JJ, Freidenberg G, Henry R, et al. Role of human skeletal muscle insulin receptor kinase in the in vivo insulin resistance of non-insulin-dependent diabetes mellitus and obesity. J Clin Endocrinol Metab 1994;78:471-7.
Caro JF, Sinha MK, Raju SM, et al. Insulin receptor kinase in human skeletal muscle from obese subjects with and without non-insulin-dependent diabetes. J Clin Invest 1987;79:1330-7.
Shao J, Catalano PM, Yamashita H, et al. Decreased insulin receptor tyrosine kinase activity and plasma cell membrane glycoprotein-1 overexpression in skeletal muscle from obese women with gestational diabetes mellitus. Diabetes 2000;49:603-10.
Ryan EA, Sullivan MJ, Skyler JS. Insulin action during pregnancy: studies with the euglycemic clamp technique. Diabetes 1985;34:380-9.
Hales CN, Barker DJP. Type 2 (non-insulin-dependent) diabetes mellitus: the Thrifty phenotype hypothesis. Diabetologia 1992;35:595-601.
Forsen T, Tuomilehto J, Reunanen A, et al. The fetal and childhood growth of persons who develop type II diabetes. Ann Intern Med 2000;33:176-82.
Dang K, Homko C, Reece EA. Factors associated with fetal macrosomia in offspring of gestational diabetic women. J Matern Fetal Med 2000;9:114-7.
Coustan DR, Imarah J. Prophylactic insulin treatment of gestational diabetes reduces the incidence of macrosomia, operative delivery, and birth trauma. Am J Obstet Gynecol 1984;150:836-42.