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      Maternal Circulating Concentrations of Tumor Necrosis Factor-Alpha, Leptin, and Adiponectin in Gestational Diabetes Mellitus: A Systematic Review and Meta-Analysis

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          Abstract

          Gestational diabetes mellitus (GDM) is one of the most common pregnancy complications. Inflammation may play a role in the pathogenesis of GDM. We performed a systematic review and meta-analysis to determine whether maternal serum concentration of tumor necrosis factor-alpha (TNF- α), leptin, and adiponectin were associated with GDM. A systematic search of PubMed and Medline was undertaken. In total, 27 trials were evaluated by meta-analyses using the software Review Manager 5.0. The results showed that maternal TNF- α ( P = 0.0003) and leptin ( P < 0.00001) concentrations were significantly higher in GDM patients versus controls. However, maternal adiponectin ( P < 0.00001) concentration was significantly lower in GDM patients compared with controls. Subgroup analysis taking in consideration the effect of obesity on maternal adipokine levels showed that circulating levels of TNF- α and leptin remained elevated in GDM patients compared to their body mass index (BMI) matched controls, and adiponectin level remained depressed in GDM individuals. Our findings strengthen the clinical evidence that GDM is accompanied by exaggerated inflammatory responses.

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          Most cited references51

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          Summary and recommendations of the Fifth International Workshop-Conference on Gestational Diabetes Mellitus.

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            Cellular mechanisms for insulin resistance in normal pregnancy and gestational diabetes.

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              Adipocytokines and the metabolic complications of obesity.

              Adipose tissue is increasingly recognized as an active endocrine organ with many secretory products and part of the innate immune system. With obesity, macrophages infiltrate adipose tissue, and numerous adipocytokines are released by both macrophages and adipocytes. Adipocytokines play important roles in the pathogenesis of insulin resistance and associated metabolic complications such as dyslipidemia, hypertension, and premature heart disease. Published literature was analyzed with the intent of addressing the role of the major adipose secretory proteins in human obesity, insulin resistance, and type 2 diabetes. This review analyzes the characteristics of different adipocytokines, including leptin, adiponectin, pro-inflammatory cytokines, resistin, retinol binding protein 4, visfatin, and others, and their roles in the pathogenesis of insulin resistance. Inflamed fat in obesity secretes an array of proteins implicated in the impairment of insulin signaling. Further studies are needed to understand the triggers that initiate inflammation in adipose tissue and the role of each adipokine in the pathogenesis of insulin resistance.
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                Author and article information

                Journal
                ScientificWorldJournal
                ScientificWorldJournal
                TSWJ
                The Scientific World Journal
                Hindawi Publishing Corporation
                2356-6140
                1537-744X
                2014
                19 August 2014
                : 2014
                : 926932
                Affiliations
                1Harbin Medical University, 157 Baojian Road, Nangang District, Harbin, Heilongjiang 150081, China
                2First Affiliated Hospital of Harbin Medical University, 199 Dazhi Street, Nangang District, Harbin, Heilongjiang 150001, China
                3Second Affiliated Hospital of Harbin Medical University, 148 Baojian Road, Nangang District, Harbin, Heilongjiang 150081, China
                Author notes

                Academic Editor: José L. Bartha

                Article
                10.1155/2014/926932
                4151523
                25202741
                07a4da6e-e391-4e7e-bb4b-5b40daa7761c
                Copyright © 2014 Jie Xu et al.

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

                History
                : 4 May 2014
                : 4 July 2014
                : 18 July 2014
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                Review Article

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