Role of insulin, adenosine, and adipokine receptors in the foetoplacental vascular dysfunction in gestational diabetes mellitus

Subiabre, Mario; Villalobos-Labra, Roberto; Silva, L.; Fuentes, Gonzalo; Toledo, Fernando; Sobrevía, Luis

doi:10.1016/j.bbadis.2018.12.021

Cited by 18 publications

(18 citation statements)

References 179 publications

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“…The effects of DM include long-term damage, dysfunction, and failure of various organs. The longterm effects of DM include progressive development of specific complications of retinopathy with potential blindness, nephropathy that may lead to renal failure, and/or neuropathy [2]. As one of the most common and sight-threatening microvascular complications of diabetes, diabetic retinopathy (DR) is the leading cause of irreversible visual loss and eye disease in people of working age worldwide [3,4].…”

Section: Introductionmentioning

confidence: 99%

Association between Aldose Reductase Gene C(-106)T Polymorphism and Diabetic Retinopathy: A Systematic Review and Meta-Analysis

Lin¹,

Peng²,

Cao³

et al. 2020

Ophthalmic Res

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Controversial results regarding the associations between aldose reductase (AR) genetic polymorphisms and diabetic retinopathy (DR) have been reported for many years. The present meta-analysis was performed to clarify the effects of the AR gene C(-106)T polymorphism on DR risk. The PubMed, Web of Sciences, Cochrane library, EMBASE, Chinese National Knowledge Infrastructure, and Wan Fang databases were extensively searched in Chinese to select relevant studies with an updated date of April 25, 2018. The Newcastle-Ottawa Scale (NOS) was applied to assess quality. The randomeffects model was applied to calculate the pooled OR and 95% CI. This meta-analysis identified 23 studies with an average score of 7.52 for NOS analysis, including 4,313 DR cases and 5,128 diabetes mellitus (DM) control cases. In the overall analysis, a significant association between the AR gene C(-106)T polymorphism and DR susceptibility was found. In subgroups stratified by DM type and ethnicity, significantly increased risks for DR were found in DM type 1, East Asian populations, and Middle Eastern populations. Compared with DR control cases, the following associations were found: T vs. C: OR 0.91, 95% CI 0.85-0.97, I 2 = 72.9%; CT + TT vs. CC: OR 0.75, 95% CI 0.68-0.81, I 2 = 86.7%; and CT vs. CC: OR 0.86, 95% CI 0.78-0.94, I 2 = 70.5%. The results of this meta-analysis showed a significant association between the AR gene C(-106)T polymorphism and susceptibility to DR in DM patients. DM patients with allele T and CT+TT genotype of the AR gene may have a lower risk of DR.

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Section: Introductionmentioning

confidence: 99%

Association between Aldose Reductase Gene C(-106)T Polymorphism and Diabetic Retinopathy: A Systematic Review and Meta-Analysis

Lin¹,

Peng²,

Cao³

et al. 2020

Ophthalmic Res

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“…Leptin metabolism and function alterations in the placenta are linked to different disorders during pregnancy, such as gestational diabetes, intrauterine growth restriction, recurrent miscarriage, and preeclampsia (Howell & Powell 2017, Briana & Malamitsi-Puchner 2020, Subiabre et al 2020. Leptin levels are also elevated in obese pregnant women correlating with more pronounced insulin resistance and activation of mTOR signaling in the placenta, that might contribute to fetal overgrowth and adiposity in the offspring (Kelly et al 2020).…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between estradiol and NFκB signaling pathways on placental leptin expression

et al. 2020

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Pregnancy success requires a proper fetal maternal interaction at the establishment of implantation. Leptin has been described as a multitasking cytokine in pregnancy, particularly in the placenta, where it acts as an autocrine hormone. The expression of leptin in normal trophoblastic cells is regulated by different endogenous signals. We have previously reported that 17β-estradiol up-regulates placental leptin expression through genomic and non-genomic mechanisms. To improve the knowledge of estrogen receptor mechanisms in regulating leptin gene expression, we examined transcription nuclear factor kappa B (NFκB) effect on estradiol leptin induction in human BeWo cell line and human term placental explants. We demonstrated that estradiol induction effect on leptin expression is blocked by the inhibition of NFκB signaling. We also found that the overexpression of p65 subunit, the active form of NFκB, induces leptin expression. Moreover, the downregulation of estrogen receptor alpha (ERα through a specific siRNA, abolished NFκB effect on leptin expression. We also demonstrated that ERα enhanced NFκB signaling pathway activation in trophoblastic cells. Estradiol treatment significantly increased p65 expression and phosphorylation of the inhibitory protein κB alpha (IκBα). A reporter plasmid containing NFκB elements was also induced in response to estradiol stimulation. Localization experiments revealed that estradiol treatment induced nuclear localization of overexpressed p65. Moreover, the overexpression of ERα produced a complete displacement of p65 protein to the nucleus. Finally, immunoprecipitation experiments showed the presence of a complex containing ERαand NFκB. All these evidences suggest a cooperative behavior between ERαand NFκB transcription factors to induce leptin transcription.

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“…Recently, many adipocyte-secreted proteins as well as adipokines have been introduced as novel links to DM [6]. It is widely accepted that the adipokines participate in many metabolic processes, including energy expenditure, appetite control, insulin sensitivity, and regulation of adipogenesis [7, 8].…”

Section: Introductionmentioning

confidence: 99%

Omentin-1 in diabetes mellitus: A systematic review and meta-analysis

et al. 2019

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ObjectivePrevious studies found inconsistent results on the relationship between diabetes mellitus and concentrations of omentin-1. This study performed a systematic review and meta-analysis to summarize previous findings on this relationship.MethodsStudies related to this outcome were obtained using a systematic search in the electronic databases of Cochrane Library, PubMed, Embase, SCOPUS, Google Scholar, gray literature and Web of Science in September 2019. The random effects model was used to measure the strength of the association between diabetes mellitus and concentrations of omentin-1, using standardized mean difference.ResultsForty-two eligible studies were included in the final meta-analysis. There was no significant difference in omentin-1 concentration between patients with type 1 diabetes mellitus and the controls. On the other hand, lower concentration levels of omentin-1 were observed in patients with gestational diabetes mellitus (standardized mean difference:-0.44, 95% confidence interval:-0.76; -0.12, p = 0.007), or type 2 diabetes mellitus (standardized mean difference: -1.74, 95% confidence interval: -2.31; -1.16, p< 0.001) than in the controls.ConclusionDecreased omentin-1 concentrations may be an important indicator for gestational diabetes mellitus and type 2 diabetes mellitus. More studies are needed to validate this hypothesis and evaluate the role of omentin-1 concentrations in type 1 diabetes mellitus.

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Role of insulin, adenosine, and adipokine receptors in the foetoplacental vascular dysfunction in gestational diabetes mellitus

Cited by 18 publications

References 179 publications

Association between Aldose Reductase Gene C(-106)T Polymorphism and Diabetic Retinopathy: A Systematic Review and Meta-Analysis

Association between Aldose Reductase Gene C(-106)T Polymorphism and Diabetic Retinopathy: A Systematic Review and Meta-Analysis

Crosstalk between estradiol and NFκB signaling pathways on placental leptin expression

Omentin-1 in diabetes mellitus: A systematic review and meta-analysis

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