P30: A humanized mouse model of gestational diabetes mellitus mimicking metabolic and immune pathologies of human pregnancy complication

2021 ◽  
Vol 85 (S1) ◽  
pp. 77-77



Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2792
Author(s):  
Monika Słupecka-Ziemilska ◽  
Piotr Wychowański ◽  
Monika Puzianowska-Kuznicka

Gestational diabetes mellitus (GDM) is the most common pregnancy complication worldwide and may result in short-term and long-term consequences for offspring. The present review highlights evidence of epigenetic programming, mostly from human studies, which occurs in offspring exposed to maternal GDM during different stages of development, paying special attention to the differences in sensitivity of offspring to maternal hyperglycemia as a result of sex-related factors. We also aim to answer the following question: If these epigenetic changes are constant throughout the lifetime of the offspring, how do they present phenotypically?



2019 ◽  
Vol 597 (18) ◽  
pp. 4689-4690
Author(s):  
N. Blysniuk ◽  
A. Visram ◽  
K. T. Lam


2022 ◽  
Vol 12 ◽  
Author(s):  
Surendra Sharma ◽  
Sayani Banerjee ◽  
Paula M. Krueger ◽  
Sandra M. Blois

Although the concepts related to fetal immune tolerance proposed by Sir Peter Medawar in the 1950s have not withstood the test of time, they revolutionized our current understanding of the immunity at the maternal-fetal interface. An important extension of the original Medawar paradigm is the investigation into the underlying mechanisms for adverse pregnancy outcomes, including recurrent spontaneous abortion, preterm birth, preeclampsia and gestational diabetes mellitus (GDM). Although a common pregnancy complication with systemic symptoms, GDM still lacks understanding of immunological perturbations associated with the pathological processes, particularly at the maternal-fetal interface. GDM has been characterized by low grade systemic inflammation that exacerbates maternal immune responses. In this regard, GDM may also entail mild autoimmune pathology by dysregulating circulating and uterine regulatory T cells (Tregs). The aim of this review article is to focus on maternal-fetal immunological tolerance phenomenon and discuss how local or systemic inflammation has been programmed in GDM. Specifically, this review addresses the following questions: Does the inflammatory or exhausted Treg population affecting the Th17:Treg ratio lead to the propensity of a pro-inflammatory environment? Do glycans and glycan-binding proteins (mainly galectins) contribute to the biology of immune responses in GDM? Our understanding of these important questions is still elementary as there are no well-defined animal models that mimic all the features of GDM or can be used to better understand the mechanistic underpinnings associated with this common pregnancy complication. In this review, we will leverage our preliminary studies and the literature to provide a conceptualized discussion on the immunobiology of GDM.



Dose-Response ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 155932582092676
Author(s):  
Weihong Feng ◽  
Yanxia Wang ◽  
Na Guo ◽  
Pu Huang ◽  
Yang Mi

Gestational diabetes mellitus (GDM) is a condition in which a hormone made by the placenta prevents the body from using insulin effectively. It is important to find an effective treatment. A mouse model of GDM was used to testify the effects of astaxanthin on glucose tolerance and insulin sensitivity. Production of inflammatory cytokines, reactive oxygen species (ROS), and glucose transporter type 4 (GLUT4) translocation and insulin-related signaling were measured in the presence of astaxanthin both in vivo and in vitro. It was found that astaxanthin improved insulin sensitivity, glucose tolerance, and litter size of offspring and reduced birth weight of offspring and inflammation in GDM mouse. Moreover, astaxanthin increased GLUT4 translocating to membrane without altering its secretion/expression and glucose uptake and consumption in C2C12 skeletal muscle cells. Furthermore, ROS generation and insulin-related signaling inhibited by tumor necrosis factor α was restored by astaxanthin. It is concluded that astaxanthin has the potential to attenuate GDM symptoms by regulating inflammation and insulin resistance in skeletal muscle of pregnant mice. Our findings suggest that astaxanthin could be a promising and effective molecule to treat GDM.



Nutrients ◽  
2017 ◽  
Vol 9 (2) ◽  
pp. 141 ◽  
Author(s):  
Jasmine Plows ◽  
Florence Budin ◽  
Rebecka Andersson ◽  
Valerie Mills ◽  
Katherine Mace ◽  
...  


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