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      Type 2 diabetes-associated genetic variants of FTO, LEPR, PPARg , and TCF7L2 in gestational diabetes in a Brazilian population

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          ABSTRACT

          Objective

          Gestational diabetes mellitus (GDM) is a metabolic disorder that shares pathophysiologic features with type 2 diabetes mellitus. The aim of this study was to investigate the association of the polymorphisms fat mass and obesity-associated (FTO) rs1421085, leptin receptor (LEPR) rs1137100, rs1137101, peroxisome proliferator-activated receptor gamma (PPARg) rs1801282, and transcription factor 7-like 2 (TCF7L2) rs7901695 with GDM.

          Subjects and methods

          252 unrelated Euro-Brazilian pregnant women were classified into two groups according to the 2015 criteria of the American and Brazilian Diabetes Association: healthy pregnant women (n = 125) and pregnant women with GDM (n = 127), matched by age. The polymorphisms were genotyped using fluorescent probes (TaqMan ®).

          Results

          All groups were in Hardy-Weinberg equilibrium. The genotype and allele frequencies of the studied polymorphisms did not show significant differences between the groups (P > 0.05). In the healthy and GDM groups, the C allele frequencies (95% CI) of the FTO rs1421085 polymorphism were 36.8% [31–43%] and 35.0% [29–41%]; the G allele frequencies (95% CI) of the LEPR rs1137100 polymorphism were 24.8% [19–30%] and 22.8% [18–28%]; the G allele frequencies (95% CI) of the LEPR rs1137101 polymorphism were 43.6% [37–50%] and 42.9% [37–49%]; the G allele frequencies (95% CI) of the PPARg rs1801282 polymorphism were 7.6% [4–11%] and 8.3% [5–12%]; and the C allele frequencies (95% CI) of the TCF7L2 rs7901695 polymorphism were 33.6% [28–39%] and 39.0% [33–45%], respectively.

          Conclusion

          The studied polymorphisms were not associated with GDM in a Brazilian population.

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          Most cited references78

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          A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.

          Obesity is a serious international health problem that increases the risk of several common diseases. The genetic factors predisposing to obesity are poorly understood. A genome-wide search for type 2 diabetes-susceptibility genes identified a common variant in the FTO (fat mass and obesity associated) gene that predisposes to diabetes through an effect on body mass index (BMI). An additive association of the variant with BMI was replicated in 13 cohorts with 38,759 participants. The 16% of adults who are homozygous for the risk allele weighed about 3 kilograms more and had 1.67-fold increased odds of obesity when compared with those not inheriting a risk allele. This association was observed from age 7 years upward and reflects a specific increase in fat mass.
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            Gestational diabetes mellitus: risks and management during and after pregnancy.

            Gestational diabetes mellitus (GDM) carries a small but potentially important risk of adverse perinatal outcomes and a long-term risk of obesity and glucose intolerance in offspring. Mothers with GDM have an excess of hypertensive disorders during pregnancy and a high risk of developing diabetes mellitus thereafter. Diagnosing and treating GDM can reduce perinatal complications, but only a small fraction of pregnancies benefit. Nutritional management is the cornerstone of treatment; insulin, glyburide and metformin can be used to intensify treatment. Fetal measurements complement maternal glucose monitoring in the identification of pregnancies that require such intensification. Glucose testing shortly after delivery can stratify the short-term diabetes risk in mothers. Thereafter, annual glucose and HbA(1c) testing can detect deteriorating glycaemic control, a harbinger of future diabetes mellitus, usually type 2 diabetes mellitus. Interventions that mitigate obesity or its metabolic effects are most potent in preventing or delaying diabetes mellitus. Lifestyle modification is the primary approach; use of medications for diabetes prevention after GDM remains controversial. Family planning enables optimization of health in subsequent pregnancies. Breastfeeding may reduce obesity in children and is recommended. Families should be encouraged to help children adopt lifestyles that reduce the risk of obesity.
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              PPAR gamma gene--a review.

              Peroxisome proliferator-activated receptor gamma (PPARγ) has been the focus of intense research because ligands for this receptor have emerged as potent insulin sensitizers used in the treatment of type 2 diabetes. There have been described three PPAR isotypes α, δ and γ which have an integrated role in controlling the expression of genes playing key roles in the storage and mobilization of lipids, in glucose metabolism, in morphogenesis and inflammatory response. Recent advances include the discovery of novel genes that are regulated by PPARγ, which helps to explain how activation of this adipocyte predominant transcription factor regulates glucose and lipid homeostasis. Increased levels of circulating free fatty acids and lipid accumulation in non-adipose tissue have been implicated in the development of insulin resistance. This situation is improved by PPARγ ligands, which promotes fatty acid storage in fat deposits and regulates the expression of adipocyte-secreted hormones that impacts on glucose homeostasis. So the net result of the pleiotropic effects of PPARγ ligands is improvement of insulin sensitivity. This review highlights the roles that PPAR gamma play in the regulation of gene expression of multiple diseases including obesity, diabetes and cancer and highlights the gene isolation transformation role. Further studies are needed for the transformation of PPAR gamma gene in plants and evaluate in animals for the treatment of type 2 diabetes.
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                Author and article information

                Journal
                Arch Endocrinol Metab
                Arch Endocrinol Metab
                aem
                Archives of Endocrinology and Metabolism
                Sociedade Brasileira de Endocrinologia e Metabologia
                2359-3997
                2359-4292
                20 March 2017
                May-Jun 2017
                : 61
                : 3
                : 238-248
                Affiliations
                [1 ] orgdiv1Departamento de Análises Clínicas orgnameUniversidade Federal do Paraná Curitiba PR Brasil originalDepartamento de Análises Clínicas, Universidade Federal do Paraná (UFPR), Curitiba, PR, Brasil
                [2 ] orgdiv1Escola de Ciências da Vida orgnamePontifícia Universidade Católica do Paraná Curitiba PR Brasil originalEscola de Ciências da Vida, Pontifícia Universidade Católica do Paraná (PUC-PR), Curitiba, PR, Brasil
                [3 ] orgdiv1Departamento de Patologia Básica orgnameUniversidade Federal do Paraná Curitiba PR Brasil originalDepartamento de Patologia Básica, Universidade Federal do Paraná (UFPR), Curitiba, PR, Brasil
                Author notes
                Correspondence to: Fabiane Gomes de Moraes Rego. Departamento de Análises Clínicas, Universidade Federal do Paraná. Rua Prefeito Lothário Meissner, 632. 80210-170 – Curitiba, PR, Brasil. rego@ 123456ufpr.br

                Disclosure: no potential conflict of interest relevant to this article was reported.

                Article
                10.1590/2359-3997000000258
                10118805
                28699988
                2e951eae-1f2d-4dbf-bcdc-1f879450e278

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 5 May 2016
                : 18 October 2016
                Page count
                Figures: 1, Tables: 4, Equations: 0, References: 69, Pages: 1
                Categories
                Articles

                diabetes,gestational diabetes mellitus,polymorphisms,genetic variants,genotype

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