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

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.

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Yucui Teng ◽  
Shuxia Xuan ◽  
Ming Jiang ◽  
Li Tian ◽  
Jinjing Tian ◽  
...  

Background. Gestational diabetes mellitus (GDM) is a severe threat to the health of both mother and child. The pathogenesis of GDM remains unclear, although much research has found that the levels of hydrogen sulfide (H2S) play an important role in complications of pregnancy. Methods. We collected venous blood samples from parturient women and umbilical vein blood (UVB) and peripheral venous blood (PVB) samples one hour after childbirth in the control, GDM-, and GDM+ groups in order to determine the concentration of glucose and H2S in plasma; to measure levels of TNF-α, IL-1β, IL-6, TGF-β1, and ADP in parturient women and the UVB of newborns; and to find the correlation of H2S with regression. Results. We found that, with the elevation of glucose, the level of H2S was decreased in GDM pregnant women and newborns and the concentrations of IL-6 and TNF-α were upregulated. With regression, IL-6 and TNF-α concentrations were positively correlated with the level of blood glucose and negatively correlated with H2S concentration. Conclusion. This study shows that downregulation of H2S participates in the pathogenesis of GDM and is of great significance in understanding the difference of H2S between normal and GDM pregnant women and newborns. This study suggests that IL-6 and TNF-α are correlated with gestational diabetes mellitus. The current study expands the knowledge base regarding H2S and provides new avenues for exploring further the pathogenesis of GDM.


2019 ◽  
Vol 56 (6) ◽  
pp. 681-689 ◽  
Author(s):  
Carmela Santangelo ◽  
Tiziana Filardi ◽  
Giuseppina Perrone ◽  
Marianna Mariani ◽  
Emanuela Mari ◽  
...  

2020 ◽  
Vol 105 (11) ◽  
Author(s):  
Anna Cinkajzlová ◽  
Kateřina Anderlová ◽  
Patrik Šimják ◽  
Zdeňka Lacinová ◽  
Jana Kloučková ◽  
...  

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.


PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e101327 ◽  
Author(s):  
Muhammad Furqan Bari ◽  
Martin O. Weickert ◽  
Kavitha Sivakumar ◽  
Sean G. James ◽  
David R. J. Snead ◽  
...  

2020 ◽  
Author(s):  
Hossein Chiti ◽  
Mohammad Hossein Izadi ◽  
Saeideh Mazloomzadeh

Insulin resistance in gestational diabetes increases maternal and fetal complications. Tumor necrosis factor-alpha (TNF-α) is an inflammatory factor associated with insulin resistance. The aim of this study was to determine the association between pregnancy serum TNF-α level and postpartum insulin resistance in patients with gestational diabetes mellitus. 50 pregnant women, including 25 cases of gestational diabetes and 25 healthy pregnant women, were evaluated. First, during the third trimester of pregnancy, serum TNF-α level of all cases were measured. Two months after delivery, based on the obtained results from insulin levels and a 2-hour glucose tolerance test, HOMA-IR and HOMA-B were calculated, and the association between serum TNF-α level and insulin resistance was determined. Data were analyzed using independent t-test, Mann-Whitney, and chi-square test in SPSS software. The mean serum level of TNF-α in women with gestational diabetes mellitus was higher than healthy subjects, but there was no significant difference between the two groups. The serum level of insulin, HOMA-IR and HOMA-B indices in women with gestational diabetes mellitus were higher than healthy subjects, with a significant difference in all of the measures between two groups (P=0.0001). There was no significant correlation between TNF-α and HOMAIR levels in insulin-resistant mothers two months after delivery (r=−0.33). Also, no significant correlation was detected between pregnancy TNF-α levels and HOMA-B index. Despite the higher serum levels of insulin, HOMA-IR, and HOMA-B in the diabetic group, the serum TNF-α level did not show any correlation with insulin resistance after delivery.


2013 ◽  
Author(s):  
Beata Matyjaszek-Matuszek ◽  
Mariusz Kowalczyk ◽  
Agnieszka Lagowska-Batyra ◽  
Wojciech Gernand ◽  
Andrzej Nowakowski ◽  
...  

2018 ◽  
Author(s):  
George Simeakis ◽  
Evangelia Vogiatzi ◽  
Panagiota Konstantakou ◽  
Evangelia Zapanti ◽  
Katerina Saltiki ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 86-LB
Author(s):  
TIANGE SUN ◽  
FANHUA MENG ◽  
RUI ZHANG ◽  
ZHIYAN YU ◽  
SHUFEI ZANG ◽  
...  

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