Gestational diabetes mellitus: an updated overview

Chiefari, Eusebio; Arcidiacono, Biagio; Foti, Daniela; Brunetti, Antonio

doi:10.1007/s40618-016-0607-5

Cited by 415 publications

(373 citation statements)

References 86 publications

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“…Gestational diabetes mellitus (GDM) which is a popular medical complication of pregnant women, can lead to the adverse maternal and fetal outcomes . GDM refers to any level of carbohydrate intolerance during the mid‐late pregnancy and the symptoms that pregnant women have not experienced before pregnancy .…”

Section: Introductionmentioning

confidence: 99%

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Xiao

Ding

Shi³

et al. 2020

J of Obstet and Gynaecol

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Aims: High-expressed miR-330-3p in gestational diabetes mellitus (GDM) patients was reported. However, the role and mechanism of miR-330-3p in GDM are rarely reported. In this research, we aim to investigate the effects of miR-330-3p on GDM. Methods: MiR-330-3p expression in the GDM patients' blood was determined by q-PCR. Blood glucose of blood samples was detected using blood glucose detection kits. Glucokinase (GCK) was confirmed to be a target gene of miR-330-3p by bioinformatics and luciferase analysis. Correlations between miR-330-3p with GCK and blood glucose were analyzed by Pearson correlation analysis. After INS-1 cells were treated with glucose and transfected with mimic, inhibitor or siGCK, GCK expression was detected by western blot, and q-PCR, enzyme-linked immunosorbent assays, cell counting kit-8 and Annexin-V/propidium iodide were conducted to examine the expression of insulin, cell viability and apoptosis. Results: MiR-330-3p was high-expressed in GDM patients' blood, while GCK was low-expressed. The miR-330-3p expression level positively correlated with blood glucoseand and it was highly expressed in glucosetreated INS-1 cells (11 and 22 mmol/L), while miR-330-3p expression negatively correlated with GCK expression. GCK expression was inhibited by miR-330-3p mimic and enhanced by the miR-330-3p inhibitor. MiR-330-3p mimic inhibited INS-1 cells' insulin expression, cell viability and induced apoptosis. Yet miR-330-3p inhibitor and siGCK exhibited opposite effects which miR-330-3p mimic and GCK played on INS-1 cells. In addition, siGCK reversed the effect of miR-330-3p inhibitor on INS-1 cells. Conclusion: Our findings proved that miR-330-3p targeting GCK lead to the dysfunction of INS-1 cells in GDM, and could become a therapeutic target for GDM treatment.

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Section: Introductionmentioning

confidence: 99%

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

Xiao

Ding

Shi³

et al. 2020

J of Obstet and Gynaecol

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“…Gestational diabetes mellitus (GDM) is one of the most common complications during pregnancy, which causes more and more burden to public health due to its increasing incidence [1]. Both the GDM pregnant women and the infants are at an elevated risk of complications, such as gestational hypertension and preeclampsia for mothers and hyperbilirubinemia, hypocalcemia, and respiratory distress syndrome for babies [2,3].…”

Section: Introductionmentioning

confidence: 99%

miR-657 Promotes Macrophage Polarization toward M1 by Targeting FAM46C in Gestational Diabetes Mellitus

Wang

Liu

et al. 2019

Mediators of Inflammation

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MicroRNA (miRNA) has been widely suggested to play a vital role of in the pathogenesis of gestational diabetes mellitus (GDM). We have previously demonstrated that miR-657 can regulate macrophage inflammatory response in GDM. However, the role of miR-657 on M1/M2 macrophage polarization in GDM pathogenesis is not clear yet. This study is aimed at elucidating this issue and identifying novel potential GDM therapeutic targets based on miRNA network. miR-657 is found to be upregulated in placental macrophages demonstrated by real-time PCR, which can enhance macrophage proliferation and migration in vitro. Luciferase reporter assay shows the evidence that FAM46C is a target of miR-657. In addition, miR-657 can promote macrophage polarization toward the M1 phenotype by downregulating FAM46C in macrophages. The present study strongly suggests miR-657 is involved in GDM pathogenesis by regulating macrophage proliferation, migration, and polarization via targeting FAM46C. miR-657/FAM46C may serve as promising targets for GDM diagnosis and treatment.

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“…Pregnancies complicated by hyperglycemia are associated with short-term and long-term risk of adverse outcomes in both mother and offspring, which includes disturbances in embryonic and fetal development, type 2 diabetes mellitus (DM2), and cardiovascular diseases [1][2][3][4]. Implications for adverse intra-uterine programming have also been largely discussed in the literature [5].…”

Section: Introductionmentioning

confidence: 99%

Hyperglycemia induces inflammatory mediators in the human chorionic villous

et al. 2018

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This study was based on the hypothesis that IL-1β and its central regulator, the inflammasome, may play a role in the inflammatory condition exhibited by placental tissues from mothers with different gestational hyperglycemia levels. Pregnant women were classified according to the glycemic reference as non-diabetic (n = 15), mild gestational hyperglycemia (n = 15), gestational diabetes mellitus (n = 15) and type 2 diabetes mellitus (n = 15). We investigated levels of pro-inflammatory factors in maternal plasma and placental tissues (by ELISA or immunohistochemistry) and, NFKB activity (by electrophoretic mobility shift assay) and inflammasome protein expression (by Western blot) in chorionic villous. Maternal plasma and placental levels of inflammatory factors (IL-1β, IL-6, and MCP-1) were increased during all hyperglycemic conditions. Villous stroma cells showed strong immunoreactivity to CD68. In addition, with syncytiotrophoblast, the villous stroma cells were also stained to detect iNOS, MCP-1, TLR2, and TLR4. Although the levels of protein had fluctuated in the groups, NLRP1, NLRP3, ASC, and Caspase 1 were up-regulated in all hyperglycemic groups suggesting the inflammasome may be assembled in these pregnant women. The NFKB activity also exhibited higher levels in hyperglycemic groups, which might imply in pro-inflammatory cytokines production. In summary, increased maternal glucose levels during pregnancy changed systemic and placental inflammatory patterns, which occurred in parallel with the expression of inflammasome factors and processing and secretion of the pro-inflammatory cytokine IL-1β. These results suggest an inflammatory condition in all gestational hyperglycemic conditions, even in hyperglycemia that is less severe than gestational or overt diabetes, likely associated with inflammasome activation and inflammatory cytokine secretion. Inflammasome activation as a possible source of inflammatory factors may be an important target to be considered while managing hyperglycemia and preventing adverse pregnancy outcomes.

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Gestational diabetes mellitus: an updated overview

Cited by 415 publications

References 86 publications

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

MiR‐330‐3p contributes to INS‐1 cell dysfunction by targeting glucokinase in gestational diabetes mellitus

miR-657 Promotes Macrophage Polarization toward M1 by Targeting FAM46C in Gestational Diabetes Mellitus

Hyperglycemia induces inflammatory mediators in the human chorionic villous

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