Cross-talk between fetal membranes and visceral adipose tissue involves HMGB1–RAGE and VIP–VPAC2 pathways in human gestational diabetes mellitus

2019 ◽  
Vol 56 (6) ◽  
pp. 681-689 ◽  
Author(s):  
Carmela Santangelo ◽  
Tiziana Filardi ◽  
Giuseppina Perrone ◽  
Marianna Mariani ◽  
Emanuela Mari ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Visceral Adipose Tissue ◽  
Cross Talk ◽  
Fetal Membranes ◽  
Visceral Adipose

scholarly journals Visceral Adipose Tissue Depth in Early Pregnancy and Gestational Diabetes Mellitus - a Cohort Study

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
João Guilherme Alves ◽  
Alex Sandro Rolland Souza ◽  
José Natal Figueiroa ◽  
Carla Adriane Leal de Araújo ◽  
Angélica Guimarães ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Cohort Study ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Visceral Adipose Tissue ◽  
Early Pregnancy ◽  
Visceral Adipose

Subclinical Inflammation and Lymphocytes in Subcutaneous and Visceral Adipose Tissue—The Influence of Pregnancy and Gestational Diabetes Mellitus

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1413-P
Author(s):  
ANNA CINKAJZLOVA ◽  
KATEřINA ANDERLOVÁ ◽  
PATRIK SIMJAK ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Visceral Adipose Tissue ◽  
Subclinical Inflammation ◽  
Visceral Adipose

Subclinical Inflammation and Adipose Tissue Lymphocytes in Pregnant Females With Gestational Diabetes Mellitus

2020 ◽  
Vol 105 (11) ◽  
Author(s):  
Anna Cinkajzlová ◽  
Kateřina Anderlová ◽  
Patrik Šimják ◽  
Zdeňka Lacinová ◽  
Jana Kloučková ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pregnant Women ◽  
Visceral Adipose Tissue ◽  
Subclinical Inflammation ◽  
Serum Samples ◽  
Pregnant Females ◽  
Visceral Adipose

Abstract Context Gestational diabetes mellitus (GDM) is accompanied by subclinical inflammation; however, little is known about local inflammation in adipose tissue and placenta. Objective To analyze systemic and local subclinical inflammation and adipose tissue lymphocyte content and phenotype in pregnant women with and without GDM. Design Observational study. Settings Academic hospital. Patients Twenty-one pregnant women with GDM (GDM group), 16 pregnant women without GDM (non-GDM group) and 15 nonpregnant control women (N group). Interventions Serum samples taken at 28 to 32 (visit 1 [V1]) and 36 to 38 (V2) gestational weeks and 6 to 12 months after delivery (V3) in the GDM and non-GDM group and before elective gynecological surgery in the N group. Subcutaneous (SAT) and visceral adipose tissue (VAT) obtained during cesarean delivery or surgery. Main Outcome Measures Serum levels and adipose tissue expression of proinflammatory cytokines, adipose tissue lymphocyte content and phenotype (for a subset of GDM and non-GDM subjects). Results Accented proinflammatory state in GDM was documented by increased circulating tumor necrosis factor-α (TNF-α) levels. In both groups of pregnant females total lymphocytes were higher in VAT compared to SAT. In GDM subjects B cells and NKT cells were higher in SAT compared to VAT and T helper cells were increased relative to SAT of non-GDM group, while no intercompartmental adipose tissue differences were seen in non-GDM women. Conclusions Pregnant females had higher total lymphocyte count in VAT relative to SAT regardless of GDM. In addition to increased systemic subclinical inflammation, GDM was associated with significant differences in lymphocyte composition between subcutaneous and visceral adipose tissue depots.

scholarly journals Cross Talk between Adipose Tissue and Placenta in Obese and Gestational Diabetes Mellitus Pregnancies via Exosomes

2017 ◽  
Vol 8 ◽  
Author(s):  
Nanthini Jayabalan ◽  
Soumyalekshmi Nair ◽  
Zarin Nuzhat ◽  
Gregory E. Rice ◽  
Felipe A. Zuñiga ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cross Talk

scholarly journals Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies

2005 ◽  
Vol 186 (3) ◽  
pp. 457-465 ◽  
Author(s):  
Martha Lappas ◽  
Kirin Yee ◽  
Michael Permezel ◽  
Gregory E Rice
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pregnant Women ◽  
Human Placenta ◽  
Fetal Membranes ◽  
Maternal Body Mass Index ◽  
Tnf Α

The aim of this study was to determine the release and regulation of leptin, resistin and adiponectin from human placenta and fetal membranes, and maternal subcutaneous adipose tissue and skeletal muscle obtained from normal and gestational diabetes mellitus (GDM)-complicated pregnancies at the time of Cesarean section. Tissue explants were incubated in the absence (basal control) or presence of 10 μg/ml lipopolysaccharide (LPS), 10, 20 or 40 ng/ml tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8, 1 μM phorbol myristate acetate, 10, 20 and 40 mM glucose, 0.1, 1 and 10 μM insulin and 0.1 1 and 10 μM dexamethasone, progesterone and estrogen. After an 18-h incubation, the medium was collected and the release of leptin, resistin and adiponectin was quantified by ELISA. Human gestational tissues and maternal tissues released immunoreactive leptin, resistin and adiponectin; however, there was no difference in the release of either resistin or adiponectin between normal pregnant women and women with gestational diabetes. The release of leptin was significantly higher in placenta, amnion and choriodecidua obtained from normal pregnant women compared with women with GDM. However, in maternal tissues, the situation was reversed, with adipose tissue and skeletal muscle obtained from women with GDM releasing significantly greater amounts of leptin. In adipose tissue and skeletal muscle the release of leptin was significantly greater in insulin-controlled GDM compared with diet-controlled GDM, and leptin release from adipose tissue was significantly correlated with maternal body mass index. In all tissues tested, there was no effect of incubation with LPS, IL-6, IL-8 or TNF-α on leptin, resistin or adiponectin release. PMA significantly increased the release of resistin from placenta and adipose tissue. Insulin increased placental resistin release, whereas the hormones dexamethasone, progesterone and estrogen significantly decreased placental resistin release. The data presented in this study demonstrate that dysregulation of leptin metabolism and/or function in the placenta may be implicated in the pathogenesis of GDM. Furthermore, resistin release is greatly affected by a variety of inflammatory mediators and hormones.

Expression of adiponectin gene and adiponectin receptors in placental and adipose tissue in women with gestational diabetes mellitus

2013 ◽  
Author(s):  
Beata Matyjaszek-Matuszek ◽  
Mariusz Kowalczyk ◽  
Agnieszka Lagowska-Batyra ◽  
Wojciech Gernand ◽  
Andrzej Nowakowski ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Adiponectin Gene ◽  
Adiponectin Receptors

scholarly journals Gestational Diabetes Mellitus and Infant Adiposity at Birth: A Systematic Review and Meta-Analysis of Therapeutic Interventions

2021 ◽  
Vol 10 (4) ◽  
pp. 835
Author(s):  
Manoja P. Herath ◽  
Jeffrey M. Beckett ◽  
Andrew P. Hills ◽  
Nuala M. Byrne ◽  
Kiran D. K. Ahuja
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fat Mass ◽  
Metabolic Disorders ◽  
Later Life ◽  
Therapeutic Interventions ◽  
Increased Risk ◽  
The Impact

Exposure to untreated gestational diabetes mellitus (GDM) in utero increases the risk of obesity and type 2 diabetes in adulthood, and increased adiposity in GDM-exposed infants is suggested as a plausible mediator of this increased risk of later-life metabolic disorders. Evidence is equivocal regarding the impact of good glycaemic control in GDM mothers on infant adiposity at birth. We systematically reviewed studies reporting fat mass (FM), percent fat mass (%FM) and skinfold thicknesses (SFT) at birth in infants of mothers with GDM controlled with therapeutic interventions (IGDMtr). While treating GDM lowered FM in newborns compared to no treatment, there was no difference in FM and SFT according to the type of treatment (insulin, metformin, glyburide). IGDMtr had higher overall adiposity (mean difference, 95% confidence interval) measured with FM (68.46 g, 29.91 to 107.01) and %FM (1.98%, 0.54 to 3.42) but similar subcutaneous adiposity measured with SFT, compared to infants exposed to normal glucose tolerance (INGT). This suggests that IGDMtr may be characterised by excess fat accrual in internal adipose tissue. Given that intra-abdominal adiposity is a major risk factor for metabolic disorders, future studies should distinguish adipose tissue distribution of IGDMtr and INGT.

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