Ultrastructure of the placenta in gestationaldiabetes mellitus

Objectives:The placenta plays critical roles during pregnancy and is essential for fetal growth and development. Its functions aredetermined by the ultrastructure of the placental barrier that is an important feature to maintain the exchange surface areabetween the fetus and the mother. Gestational diabetes mellitus (GDM) comprises unfit conditions for embryonic and feto-placental development, and may result in placental abnormalities. The aim of this study was to detect the ultrastructural changes ofthe placenta in women with GDM. Methods: The placentas of 10 women with GDM without pregestational diabetics, hypertension and chronic diseases and10 controls were studied. Six control women were delivered vaginally and the remaining cases by caesarian section at a gestational age of 36 to 39 weeks. Placental samples were measured for their thickness and prepared for light and transmission electron microscopy study. Results: Light microscopic study of the control placentas showed numerous densely packed microvilli with syncytial knots andthin-walled blood vessels and wide intervillous spaces. The placentas of GDM cases showed reduced number of microvilli withsyncytial knots, thick-walled vessels, edematous spaces, areas of fibrosis and perivillous fibrinoid degeneration. Electron microscopic study of the placentas of the control women showed terminal villi with a thick layer of syncytiotrophoblasts (Sy) with a lotof regular cylindrical microvilli and a thin layer of cytotrophoblasts (Cy). There were some endoplasmic reticulum cisternae besidesfew mitochondria. The underlying villus core was harboring fetal capillaries lined with flat endothelial cells and thin basementmembrane. There was no fibrosis or edema. In the placenta of GDM women, there was hypertrophy of Cy with atrophy of Sywith multiple vacuoles and areas for glycogen storage. The subtrophoblastic membrane was thick and the microvilli were scarce.The villous core showed congested capillaries, stromal macrophages, edematous spaces, glycogen storage areas and fibrosis. Conclusion:All the changes in placentas of gestational diabetes were attributed to associated hypoxia and oxidative stress dueto decreased uteroplacental flow that was aggravated by the thick placental barrier and the presence of edema, fibrosis and glycogen storage areas that increased the distance of transfer between the fetus and mother

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Gül M, Bayat N, Çetin A, Kepekçi RA, Şimflek Y, Kayhan B, Turhan U, Otlu A. Histopathological, ultrastructural and apoptotic changes in diabetic rat placenta. Balkan Med J 2015;32:296-302.

Meng Q, Shao L, Luo L, Mu Y, Xu W, Gao C, Gao L, Liu J, Cui Y. Ultrastructure of placenta of gravidas with gestational diabetes mellitus. Obstet Gynecol Int 2015;2015:283124.

Aires MB, Dos Santos AC. Effects of maternal diabetes on tro- phoblast cells. World J Diabetes 2015;6:338-44.

Castellucci M, Kaufmann P. Basic structure of the villous trees. In: Benirschke K, Kaufmann P, Baergen RN, editors. Pathology of the human placenta. 5th ed. New York (NY): Springer; 2006. p. 50-120.

American Diabetes Association. Standards of medical care in dia- betes-2011. Diabetes Care 2011;34:S11-61.

Zhang F, Dong L, Zhang CP, Li B, Wen J, Gao W, Sun S, Lv F, Tian H, Tuomilehto J, Qi L, Zhang CL, Yu Z, Yang X, Hu G. Increasing prevalence of gestational diabetes mellitus in Chinese women from 1999 to 2008. Diabet Med 2011;28:652-7.

Desoye G, Hauguel-de Mouzon S. The human placenta in gesta- tional diabetes mellitus. The insulin and cytokine network. Diabetes Care 2007;30 Suppl 2:S120-6.

Gheorman L, Pleflea IE, Gheorman V. Histopathological considera- tions of placenta in pregnancy with diabetes. Rom J Morphol Embryol 2012;53:329-36.

Hayat MA. Principles and techniques of electron microscopy: bio- logical applications. 3rd ed. New York (NY): CRC Press; 1989. p. 24-74.

Gude NM, Roberts CT, Kalionis B, King RG. Growth and function of the normal human placenta. Thromb Res 2004;114:397-407.

Lemasters JJ, Theruvath TP, Zhong Z, Nieminen AL. Mitochondrial calcium and the permeability transition in cell death. Biochim Biophys Acta 2009;1787:1395-401.

Pagliarini DJ, Calvo SE, Chang B, Sheth SA, Vafai SB, Ong SE, Walford GA, Sugiana C, Boneh A, Chen WK, Hill DE, Vidal M, Evans JG, Thorburn DR, Carr SA, Mootha VK. A mitochondrial protein compendium elucidates complex I disease biology. Cell 2008; 134:112-23.

Slukvin II, Salamat MS, Chandra S. Morphologic studies of the pla- centa and autopsy findings in neonatal-onset glutaric acidemia type II. Pediatr Dev Pathol 2002;5:315-21.

Zorn TM, Zuniga M, Madrid E, Tostes R, Fortes Z, Giachini F, San Martín S. Maternal diabetes affects cell proliferation in developing rat placenta. Histol Histopathol 2011;26:1049-56.

Mayhew TM, Sampson C. Maternal diabetes mellitus is associated with altered deposition of fibrin-type fibrinoid at the villous surface in term placentae. Placenta 2003;24:524-31.

Joshi M, Kotha SR, Malireddy S, Selvaraju V, Satoskar AR, Palesty A, McFadden DW, Parinandi NL, Maulik N. Conundrum of pathogen- esis of diabetic cardiomyopathy: role of vascular endothelial dysfunc- tion, reactive oxygen species, and mitochondria. Mol Cell Biochem 2014;386:233-49.

Frohlich JD, Huppertz B, Abuja PM, König J, Desoye G. Oxygen modulates the response of first-trimester trophoblasts to hyper- glycemia. Am J Pathol 2012;180:153-64.

Jauniaux E, Burton GJ. The role of oxidative stress in placental-relat- ed diseases of pregnancy. J Gynecol Obstet Biol Reprod (Paris) 2016; 45:775-85.

Magee TR, Ross MG, Wedekind L, Desai M, Kjos S, Belkacemi L. Gestational diabetes mellitus alters apoptotic and inflammatory gene expression of trophobasts from human term placenta. J Diabetes Complications 2014;28:448-59.

Kobayashi S. Choose delicately, reuse adequately: the newly recycled process of autophagy. Biol Pharm Bull 2015;38:1098-103.

Curtis S, Jones CJ, Garrod A, Hulme CH, Heazell AE. Identification of autophagic vacuoles and regulators of autophagy in villous tro- phoblast from normal term pregnancies and in fetal growth restric- tion. J Matern Fetal Neonatal Med 2013;26:339-46.

Holmes VA, Young IS, Patterson CC, Pearson DW, Walker JD, Maresh MJ, McCance DR. Optimal glycemic control, pre-eclampsia, and gestational hypertension in women with type 1 diabetes in the dia- betes and pre-eclampsia intervention trial. Diabetes Care 2011;34: 1683-8.

Gauster M, Desoye G, Tötsch M, Hiden U. The placenta and ges- tational diabetes mellitus. Curr Diab Rep 2012;12:16-23.

Shapiro F, Mulhern H, Weis MA, Eyre D. Rough endoplasmic reticulum abnormalities in a patient with spondyloepimetaphyseal dysplasia with scoliosis, joint laxity and finger deformities. Ultrastruct Pathol 2006;30:393-400.

Yoruk M, Kanter M, Meral I, Agaoglu Z. Localization of glycogen in the placenta and fetal and maternal livers of cadmium-exposed diabetic pregnant rats. Biol Trace Elem Res 2003;96:217-26.

Padmanabhan R, Shafiullah M. Intrauterine growth retardation in experimental diabetes: possible role of the placenta. Arch Physiol Biochem 2001;109:260-71.

Shams F, Rafique M, Samoo NA, Irfan R. Fibrinoid necrosis and hyalinization observed in normal, diabetic and hypertensive pla- centae. J Coll Physicians Surg Pak 2012;22:769-72.

Jarmuzek P, Wielgos M, Bomba-Opon D. Placental pathologic changes in gestational diabetes mellitus. Neuro Endocrinol Lett 2015;36:101-5.

Gabbay-Benziv R, Baschat AA. Gestational diabetes as one of the "great obstetrical syndromes" - the maternal, placental, and fetal dialog. Best Pract Res Clin Obstet Gynaecol 2015;29:150-5.

Augustine G, Pulikkathodi M, Renjith S, Jithesh TK. A study of pla- cental histological changes in gestational diabetes mellitus on account of fetal hypoxia. Int J Med Sci Public Health 2016;5:2457-60.

Guo J, Nguyen A, Banyard DA, Fadavi D, Toranto JD, Wirth GA, Paydar KZ, Evans GR, Widgerow AD. Stromal vascular fraction: a regenerative reality? Part 2: mechanism of regenerative action. J Plast Reconstr Aesthet Surg 2016;69:180-8.