Gestational diabetes mellitus and the ghrelin system

Brink, H S; Lely, Aart Jan van der; Delhanty, Patric J. D.; Huisman, Martin; Linden, Joke van der

doi:10.1016/j.diabet.2017.10.013

Cited by 5 publications

(5 citation statements)

References 9 publications

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“…Ghrelin, a 28-amino acid peptide, is encoded by the preproghrelin gene Ghrl and primarily secreted by entero-endocrine cells of the gastrointestinal tract and hypothalamus [132,133]. During pregnancy, ghrelin levels in maternal circulation are decreased [134,135], probably as a result of adaptation processes reflected by insulin resistance, and pituitary GH substitution by placental GH [55].…”

Section: Blood Levels Of Ghrelin and Fetal Growthmentioning

confidence: 99%

Diabetes during Pregnancy: A Maternal Disease Complicating the Course of Pregnancy with Long-Term Deleterious Effects on the Offspring. A Clinical Review

Ornoy

Becker

Weinstein-Fudim³

et al. 2021

IJMS

168

101

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In spite of the huge progress in the treatment of diabetes mellitus, we are still in the situation that both pregestational (PGDM) and gestational diabetes (GDM) impose an additional risk to the embryo, fetus, and course of pregnancy. PGDM may increase the rate of congenital malformations, especially cardiac, nervous system, musculoskeletal system, and limbs. PGDM may interfere with fetal growth, often causing macrosomia, but in the presence of severe maternal complications, especially nephropathy, it may inhibit fetal growth. PGDM may also induce a variety of perinatal complications such as stillbirth and perinatal death, cardiomyopathy, respiratory morbidity, and perinatal asphyxia. GDM that generally develops in the second half of pregnancy induces similar but generally less severe complications. Their severity is higher with earlier onset of GDM and inversely correlated with the degree of glycemic control. Early initiation of GDM might even cause some increase in the rate of congenital malformations. Both PGDM and GDM may cause various motor and behavioral neurodevelopmental problems, including an increased incidence of attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Most complications are reduced in incidence and severity with the improvement in diabetic control. Mechanisms of diabetic-induced damage in pregnancy are related to maternal and fetal hyperglycemia, enhanced oxidative stress, epigenetic changes, and other, less defined, pathogenic mechanisms.

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Section: Blood Levels Of Ghrelin and Fetal Growthmentioning

confidence: 99%

Diabetes during Pregnancy: A Maternal Disease Complicating the Course of Pregnancy with Long-Term Deleterious Effects on the Offspring. A Clinical Review

Ornoy

Becker

Weinstein-Fudim³

et al. 2021

IJMS

168

101

View full text Add to dashboard Cite

show abstract

“…The prevalence of GDM ranging from 8.9 to 53.4% in the world and is rising every year . Although the pathophysiological mechanisms of GDM have not been fully elucidated, it was well known that the insufficient adaptability of pancreatic β cell to insulin resistance, which is characterized by mid‐late pregnancy, maybe the primary cause of GDM . During normal pregnancy, the stability of glucose in pregnant women depends on the physiological accumulation of insulin secretion; furthermore, this compensatory accumulation is closely related to the biological functions of pancreatic β cells: it is speculated that several regulatory molecules, such as cell growth regulator, which can regulate the biological function of the pancreatic β cell, play a crucial effect in these adaptive changes to meet these compensatory requirements .…”

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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“…Inadequate adaptation to insulin resistance in pancreatic β-cells is the main cause of GDM. 40,41 Physiological secretion of insulin is essential for the maintenance of glucose levels during pregnancy, and this compensatory accumulation and biological functions of pancreatic cells have been widely used to study GDM in vitro. 38,42,43 Li et al…”

Section: Discussionmentioning

confidence: 99%

Role of lncRNA‐MEG8/miR‐296‐3p axis in gestational diabetes mellitus

et al. 2022

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Aim Gestational diabetes mellitus (GDM) is the most common complication in pregnancy. This study aimed to investigate the potential mechanism and effects of long‐noncoding RNA maternally expressed 8 (lncRNA‐MEG8) in GDM. Methods Targeted interactions involving lncRNA‐MEG8 and miR‐296‐3p were initially predicted using starBase software and then confirmed using dual‐luciferase reporter gene analysis. The expression levels of lncRNA‐MEG8 and miR‐296‐3p in peripheral blood samples from patients with GDM were measured using reverse transcription‐quantitative polymerase chain reaction. Enzyme‐linked immunosorbent assay was used to evaluate the overall levels of insulin and insulin secretion. Additionally, MTT and flow cytometric methods were used to detect cell viability and apoptosis. Cell apoptosis‐associated proteins were determined by western blotting. Results Our results indicated that lncRNA‐MEG8 is a potential target of miR‐296‐3p. lncRNA‐MEG8 level was higher, whereas that of miR‐296‐3p was lower in patients with GDM than in healthy individuals. LncRNA‐MEG8‐siRNA promoted insulin content and secretion. Furthermore, MEG8‐siRNA increased cell viability and decreased apoptosis. However, these changes were reversed by an miR‐296‐3p inhibitor. Moreover, a miR‐296‐3p mimic had the same effect on INS‐1 cells as MEG8‐siRNA, as evidenced by enhanced insulin secretion, cell viability, and reduced apoptosis. Conclusion LncRNA‐MEG8‐siRNA promotes pancreatic β‐cell function by upregulating miR‐296‐3p.

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Gestational diabetes mellitus and the ghrelin system

Cited by 5 publications

References 9 publications

Diabetes during Pregnancy: A Maternal Disease Complicating the Course of Pregnancy with Long-Term Deleterious Effects on the Offspring. A Clinical Review

Diabetes during Pregnancy: A Maternal Disease Complicating the Course of Pregnancy with Long-Term Deleterious Effects on the Offspring. A Clinical Review

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

Role of lncRNA‐MEG8/miR‐296‐3p axis in gestational diabetes mellitus

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