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

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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Analysis of phosphatidylinositol 3-kinase activation in the adipose tissue of gestational diabetes mellitus patients and insulin resistance

Journal of Huazhong University of Science and Technology [Medical Sciences] ◽

10.1007/s11596-010-0458-9 ◽

2010 ◽

Vol 30 (4) ◽

pp. 505-508 ◽

Cited By ~ 3

Author(s):

Yongli Chu ◽

Wenjuan Liu ◽

Qing Cui ◽

Guijiao Feng ◽

Yan Wang ◽

...

Keyword(s):

Diabetes Mellitus ◽

Insulin Resistance ◽

Adipose Tissue ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Phosphatidylinositol 3 Kinase ◽

Kinase Activation ◽

Phosphatidylinositol 3

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Epigenetic Alterations Related to Gestational Diabetes Mellitus

International Journal of Molecular Sciences ◽

10.3390/ijms22179462 ◽

2021 ◽

Vol 22 (17) ◽

pp. 9462

Author(s):

Jorge Valencia-Ortega ◽

Renata Saucedo ◽

Martha A. Sánchez-Rodríguez ◽

José G. Cruz-Durán ◽

Edgar G. Ramos Martínez

Keyword(s):

Diabetes Mellitus ◽

Adipose Tissue ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Maternal Blood ◽

Future Research ◽

Epigenetic Alterations ◽

Future Health ◽

Micro Rnas ◽

Metabolic Complication

Gestational diabetes mellitus (GDM) is the most common metabolic complication in pregnancy, which affects the future health of both the mother and the newborn. Its pathophysiology involves nutritional, hormonal, immunological, genetic and epigenetic factors. Among the latter, it has been observed that alterations in DNA (deoxyribonucleic acid) methylation patterns and in the levels of certain micro RNAs, whether in placenta or adipose tissue, are related to well-known characteristics of the disease, such as hyperglycemia, insulin resistance, inflammation and excessive placental growth. Furthermore, epigenetic alterations of gestational diabetes mellitus are observable in maternal blood, although their pathophysiological roles are completely unknown. Despite this, it has not been possible to determine the causes of the epigenetic characteristics of GDM, highlighting the need for integral and longitudinal studies. Based on this, this article summarizes the most relevant and recent studies on epigenetic alterations in placenta, adipose tissue and maternal blood associated with GDM in order to provide the reader with a general overview of the subject and indicate future research topics.

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The association of circulating adiponectin and + 45 T/G polymorphism of adiponectin gene with gestational diabetes mellitus in Iranian population

Journal of Diabetes & Metabolic Disorders ◽

10.1186/s40200-015-0156-z ◽

2015 ◽

Vol 14 (1) ◽

Cited By ~ 11

Author(s):

Mohammad Ali Takhshid ◽

Zinab Haem ◽

Farzaneh Aboualizadeh

Keyword(s):

Diabetes Mellitus ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Iranian Population ◽

Adiponectin Gene

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Differential Expression of MicroRNAs in Omental Adipose Tissue From Gestational Diabetes Mellitus Subjects Reveals miR-222 as a Regulator of ERα Expression in Estrogen-Induced Insulin Resistance

Endocrinology ◽

10.1210/en.2013-2046 ◽

2014 ◽

Vol 155 (5) ◽

pp. 1982-1990 ◽

Cited By ~ 69

Author(s):

Zhonghua Shi ◽

Chun Zhao ◽

Xirong Guo ◽

Hongjuan Ding ◽

Yugui Cui ◽

...

Keyword(s):

Diabetes Mellitus ◽

Insulin Resistance ◽

Adipose Tissue ◽

Gestational Diabetes ◽

Gestational Diabetes Mellitus ◽

Differential Expression ◽

Molecular Mechanisms ◽

Expression Patterns ◽

Luciferase Assay ◽

Omental Adipose Tissue

Omental adipose tissue plays a central role in insulin resistance in gestational diabetes mellitus (GDM), and the molecular mechanisms leading to GDM remains vague. Evidence demonstrates that maternal hormones, such as estradiol, contribute to insulin resistance in GDM. In this study we determined the differential expression patterns of microRNAs (miRNAs) in omental adipose tissues from GDM patients and pregnant women with normal glucose tolerance using AFFX miRNA expression chips. MiR-222, 1 of 17 identified differentially expressed miRNAs, was found to be significantly up-regulated in GDM by quantitative real-time PCR (P < .01), and its expression was closely related with serum estradiol level (P < .05). Furthermore, miR-222 expression was significantly increased in 3T3-L1 adipocytes with a high concentration of 17β-estradiol stimulation (P < .01), whereas the expressions of estrogen receptor (ER)-α protein and insulin-sensitive membrane transporter glucose transporter 4 (GLUT4) protein (P < .01) were markedly reduced. In addition, ERα was shown to be a direct target of miR-222 in 3T3-L1 adipocytes by using the luciferase assay. Finally, antisense oligonucleotides of miR-222 transfection was used to silence miR-222 in 3T3-L1 adipocytes. The results showed that the expressions of ERα and GLUT4, the insulin-stimulated translocation of GLUT4 from the cytoplasm to the cell membrane and glucose uptake in mature adipocytes were dramatically increased (P < .01). In conclusion, miR-222 is a potential regulator of ERα expression in estrogen-induced insulin resistance in GDM and might be a candidate biomarker and therapeutic target for GDM.

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