Placental structure in gestational diabetes mellitus.

Clicks: 385
ID: 13624
2019
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Abstract
The placenta is a transitory organ, located between the mother and the foetus, which supports intrauterine life. This organ has nutritional, endocrine and immunologic functions to support foetal development. Several factors are related to the correct functioning of the placenta including foetal and maternal blood flow, appropriate nutrients, expression and function of receptors and transporters, and the morphology of the placenta itself. Placental morphology is crucial for understanding the pathophysiology of the organ as represents the physical structure where nutrient exchange occurs. In pathologies of pregnancy such as diabetes mellitus in humans and animal models, several changes in the placental morphology occur, related mainly with placental size, hypervascularization, higher branching capillaries of the villi and increased glycogen deposits among others. Gestational diabetes mellitus is associated with modifications in the structure of the human placenta including changes in the surface area and volume, as well as histological changes including an increased volume of intervillous space and terminal villi, syncytiotrophoblast number, fibrinoid areas, and glycogen deposits. These modifications may result in functional changes in this organ thus limiting the wellbeing of the developing foetus. This review gives an overview of recurrent morphological changes at macroscopic and histological levels seen in the placenta from gestational diabetes in humans and animal models. This article is part of a Special Issue entitled: Membrane Transporters and Receptors in Pregnancy Metabolic Complications edited by Luis Sobrevia.
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carrascowong2019placentalbiochimica Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Carrasco-Wong, Ivo;Moller, Alejandra;Giachini, Fernanda R;Lima, Victor V;Toledo, Fernando;Stojanova, Jana;Sobrevia, Luis;Martín, Sebastián San;
Journal biochimica et biophysica acta molecular basis of disease
Year 2019
DOI
S0925-4439(19)30258-3
URL
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