Micro‐ribonucleic acid‐binding site variants of type 2 diabetes candidate loci predispose to gestational diabetes mellitus in Chinese Han women

Wang, Xiaojing; Li, Wei; Ma, Liangkun; Ping, Fan; Liu, Juntao; Wu, Xueyan; Mao, Jiangfeng; Wang, Xi; Nie, Min

doi:10.1111/jdi.12803

Cited by 7 publications

(4 citation statements)

References 41 publications

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“…Notwithstanding, during pregnancy the percentage of β-cells expressing PAX4 transiently increases correlating with a higher proliferation of β-cells, highlighting the role of this transcription factor in the adaptation processes that take place during gestation to compensate for the increased insulin resistance [86]. In agreement with this, recent studies have associated SNPs near or within the PAX4 gene with GDM [96,97]. Based on the importance of PAX4 on β-cell formation and plasticity, we can presume that women harboring detrimental mutations in this transcription factor will likely have a reduced β-cell mass with a blunted adaptive response to the increase in insulin resistance, rendering these women more susceptible to develop GDM.…”

Section: Pax4 a Master Regulator Of β-Cell Phenotype And Plasticity mentioning

confidence: 65%

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Lorenzo

Martín-Montalvo

Vuilleumier

et al. 2019

IJMS

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Gestational diabetes mellitus (GDM), a metabolic disease that develops with the increase in insulin resistance during late pregnancy, is currently one of the most common complications affecting pregnancy. The polygenic nature of GDM, together with the interplay between different genetic variants with nutritional and environmental factors has hindered the full understanding of the etiology of this disease. However, an important genetic overlap has been found with type 2 diabetes mellitus (T2DM) and, as in the case of T2DM, most of the identified loci are associated with β-cell function. Early detection of GDM and adequate interventions to control the maternal glycemia are necessary to avoid the adverse outcomes for both the mother and the offspring. The in utero exposure to the diabetic milieu predispose these children for future diseases, among them T2DM, originating a vicious circle implicated in the increased prevalence of both GDM and T2DM. The involvement of inflammatory processes in the development of GDM highlights the importance of pancreatic β-cell factors able to favor the adaptation processes required during gestation, concomitantly with the protection of the islets from an inflammatory milieu. In this regard, two members of the Pax family of transcription factors, PAX4 and PAX8, together with the chromatin remodeler factor HMG20A, have gained great relevance due to their involvement in β-cell mass adaptation together with their anti-inflammatory properties. Mutations in these factors have been associated with GDM, highlighting these as novel candidates for genetic screening analysis in the identification of women at risk of developing GDM.

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Section: Pax4 a Master Regulator Of β-Cell Phenotype And Plasticity mentioning

confidence: 65%

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Lorenzo

Martín-Montalvo

Vuilleumier

et al. 2019

IJMS

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“…In support of this suggestion, Wang et al (33) indicated that miR-binding-single nucleotide polymorphisms in T2DM candidate loci were associated with GDM susceptibility and supposed that a similar genetic basis for GDM and T2DM.…”

Section: Discussion:-mentioning

confidence: 94%

Reciprocal Relationship Between Insulin Resistance and Disturbed Adma/No Axis in Gestational Diabetes Mellitus.

MD¹,

MD²,

MD³

2018

IJAR

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Objectives: To estimate serum nitric oxide (NO) and asymmetric dimethylarginine (ADMA) levels in pregnant women and correlate it with severity of gestational diabetes mellitus (GDM) judged by Oral Glucose Tolerance Test (OGTT). Patients & Methods: 225 pregnant women gave fasting blood samples to estimate baseline blood glucose (BG), and serum insulin, NO and ADMA, and to undergo OGTT. Insulin resistance (IR) was indicated by HOMA-IR score >2. At 24 th week, blood sample were re-evaluated using OGTT and women were categorized in Study (GDM) and Control (free of GDM) group. Results: At 24 th week, HOMA-IR scores were significantly higher than baseline scores and in study versus control women. Baseline serum ADMA levels were significantly higher, while serum NO levels were significantly lower in study versus control women and correlated with body mass index (BMI), GDM, BG and HOMA-IR score of all women. Serum ADMA and NO showed significant correlation with extent of serum insulin change, but low serum NO is significant predictor for development and severity of IR. Conclusion: IR induces endothelial dysfunction manifested as low serum NO and high serum ADMA. Baseline serum NO could predict the extent of serum insulin change.

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“…The observation that the adaptor AP1 and retromer play opposing roles in trafficking of sortilin between the Golgi apparatus and lysosomes was one of the first hints that retromer could function in trafficking pathways germane to GLUT4 [55]. The retromer subunit Vps26 is associated with T2DM in South Asian populations [56], and genome-wide association and other studies have further piqued interest in retromer in the context of diabetes [57,58]. Using a human adipocyte cell line, Yang et al showed that retromer components Vps26, Vps35, and SNX27 colocalise with intracellular GLUT4 and exhibit insulin-dependent translocation to the PM [59].…”

Section: Trends Trends In In Cell Biology Cell Biologymentioning

confidence: 99%

Building GLUT4 Vesicles: CHC22 Clathrin’s Human Touch

Gould

Brodsky

Bryant

2020

Trends in Cell Biology

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Insulin stimulates glucose transport by triggering regulated delivery of intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane. This process is defective in diseases such as type 2 diabetes (T2DM). While studies in rodent cells have been invaluable in understanding GLUT4 traffic, evolutionary plasticity must be considered when extrapolating these findings to humans. Recent work has identified species-specific distinctions in GLUT4 traffic, notably the participation of a novel clathrin isoform, CHC22, in humans but not rodents. Here, we discuss GLUT4 sorting in different species and how studies of CHC22 have identified new routes for GLUT4 trafficking. We further consider how different sorting-protein complexes relate to these routes and discuss other implications of these pathways in cell biology and disease. HighlightsInsulin stimulates glucose transport in fat and muscle cells by triggering the regulated delivery of GLUT4-containing IRVs to the cell surface.GLUT4 trafficking in human cells involves the noncanonical clathrin isoform CHC22 that sorts GLUT4 to the GSC. CHC22 clathrin is not expressed in rodents where different mechanisms underlie GLUT4 trafficking.New work has shown that CHC22clathrin directs newly synthesised GLUT4 from the ER-Golgi intermediate compartment to the GSC without transit through the Golgi, in addition to mediating endosomal sorting of GLUT4.CHC22 clathrin interacts with p115, sortilin, IRAP, and GGA2 to mediate these distinct trafficking pathways.CHC22 clathrin enhances GLUT4 sequestration in human cells and is crucial for insulin-stimulated glucose transport.The newly identified CHC22-dependent pathway from the ERGIC could also operate in other cell types to control the delivery of cargo to specialised organelles.

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Micro‐ribonucleic acid‐binding site variants of type 2 diabetes candidate loci predispose to gestational diabetes mellitus in Chinese Han women

Cited by 7 publications

References 41 publications

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus

Reciprocal Relationship Between Insulin Resistance and Disturbed Adma/No Axis in Gestational Diabetes Mellitus.

Building GLUT4 Vesicles: CHC22 Clathrin’s Human Touch

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