Laboratory of reproduction and metabolism cefybo-conicet. Faculty of Medicine, UBA
DOI:
https://doi.org/10.47196/diab.v51i1.48Keywords:
reproduction, metabolism, macrosomiaAbstract
In pregnancy, the complications induced by pregestational and gestational diabetes are multiple. They include alterations that can affect the early embryo and lead to implantation failures, anomalies in early organogenesis processes that increase the risk of congenital malformations and failures in the placental development processes that can be linked both to the greater induction of preeclampsia and to intrauterine growth anomalies (growth retardation or macrosomia) that affect perinatal and postnatal development. In this context, the metabolic alterations characteristic of maternal diabetes are relevant, both the metabolism of carbohydrates and lipids, and which will impact the transfer of nutrients to the fetus and affect fetal development and growth. The adverse consequences occur in the mother (where the complications of diabetes are compounded by the strong impact of the adaptive changes of pregnancy), in embryonic, placental and fetal development, in perinatal complications and in the life of the mother. neonate, in which the risk of programming metabolic and cardiovascular alterations is high.
References
McCance DR. Diabetes in pregnancy. Best Pract Res Clin Obstet Gynaecol 2015; 29:685-99.
Hod M, Kapur A, Sacks DA, Hadar E, Agarwal M, Di Renzo GC, et al. The International Federation of Gynecology and Obstetrics (FIGO). Initiative on gestational diabetes mellitus: a pragmatic guide for diagnosis, management and care. Int J Gynaecol Obstet 2015; 131 Suppl 3:S173.
Lappas M, Hiden U, Desoye G, Froehlich J, Hauguel-de Mouzon S, Jawerbaum A. The role of oxidative stress in the pathophysiology of gestational diabetes mellitus. Antioxid Redox Signal 2011; 15:3061-100.
Mitanchez D, Yzydorczyk C, Simeoni U. What neonatal complications should the pediatrician be aware of in case of maternal gestational diabetes? World J Diabetes 2015; 6:734-43.
Jawerbaum A, White V. Animal models in diabetes and pregnancy. Endocr Rev 2010; 31:680-701.
Jawerbaum A, González E. Diabetic pregnancies: the challenge of developing in a pro-inflammatory environment. Curr Med Chem 2006; 13:2127-38.
Capobianco E, Pelesson M, Careaga V, Fornes D, Canosa I, Higa R, et al. Intrauterine programming of lipid metabolic alterations in the heart of the offspring of diabetic rats is prevented by maternal diets enriched in olive oil. Mol Nutr Food Res 2015; 59:1997-2007.
Capobianco E, White V, Sosa M, Marco ID, Basualdo MN, Faingold MC, et al. Regulation of matrix metalloproteinases 2 and 9 activities by peroxynitrites in term placentas from type 2 diabetic patients. Reprod Sci 2012; 19:814-22.
Wahli W, Michalik L. PPARs at the crossroads of lipid signaling and inflammation. Trends Endocrinol Metab 2012; 23:351-63.
Jawerbaum A, Capobianco E. Review: effects of PPAR activation in the placenta and the fetus: implications in maternal diabetes. Placenta 2011; 32 Suppl 2:S212-7.
Higa R, González E, Pustovrh MC, White V, Capobianco E, Martínez N, et al. PPARdelta and its activator PGI2 are reduced in diabetic embryopathy: involvement of PPARdelta activation in lipid metabolic and signalling pathways in rat embryo early organogenesis. Mol Hum Reprod 2007; 13:103-10.
Pustovrh MC, Capobianco E, Martínez N, Higa R, White V, Jawerbaum A. MMP/TIMP balance is modulated in vitro by 15dPGJ(2) in fetuses and placentas from diabetic rats. Eur J Clin Invest 2009; 39:1082-90.
Martínez N, Capobianco E, White V, Pustovrh MC, Higa R, Jawerbaum A. Peroxisome proliferator-activated receptor alpha activation regulates lipid metabolism in the feto-placental unit from diabetic rats. Reproduction 2008; 136:95-103.
Capobianco E, Martínez N, Fornes D, Higa R, Di Marco I, Basualdo MN, et al. PPAR activation as a regulator of lipid metabolism, nitric oxide production and lipid peroxidation in the placenta from type 2 diabetic patients. Mol Cell Endocrinol 2013; 377:7-15.
Kurtz M, Capobianco E, Martínez N, Roberti SL, Arany E, Jawerbaum A. PPAR ligands improve impaired metabolic pathways in fetal hearts of diabetic rats. J Mol Endocrinol 2014; 53:237-46.
Capobianco E, Fornes D, Linenberg I, Powell TL, Jansson T, Jawerbaum A. A novel rat model of gestational diabetes induced by intrauterine programming is associated with alterations in placental signaling and fetal overgrowth. Mol Cell Endocrinol 2016; 422:221-32.
Mazzucco MB, Fornes D, Capobianco E, Higa R, Jawerbaum A, White V. Maternal saturated-fat-rich diet promotes leptin resistance in fetal liver lipid catabolism and programs lipid homeostasis impairments in the liver of rat offspring. J Nutr Biochem 2016; 27:61-9.
Jawerbaum A, White V. Review on intrauterine programming: consequences in rodent models of mild diabetes and mild fat overfeeding are not mild. Placenta 2017; 52:21-32.
Downloads
Published
How to Cite
Issue
Section
License
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Dirección Nacional de Derecho de Autor, Exp. N° 5.333.129. Instituto Nacional de la Propiedad Industrial, Marca «Revista de la Sociedad Argentina de Diabetes - Asociación Civil» N° de concesión 2.605.405 y N° de disposición 1.404/13.
La Revista de la SAD está licenciada bajo Licencia Creative Commons Atribución – No Comercial – Sin Obra Derivada 4.0 Internacional.
Por otra parte, la Revista SAD permite que los autores mantengan los derechos de autor sin restricciones.
