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      Glucose metabolism-related gene polymorphisms as the risk predictors of type 2 diabetes

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          Abstract

          Type 2 diabetes mellitus (T2DM) is a complex polygenic metabolic disease characterized by elevated blood glucose. Multiple environmental and genetic factors can increase the risk of T2DM and its complications, and genetic polymorphisms are no exception. This review is mainly focused on the related genes involved in glucose metabolic, including G6PC2, GCK, GCKR and OCT3. In this review, we have summarized the results reported globally and found that the genetic variants of GCK and OCT3 genes is a risk factor for T2DM while G6PC2 and GCKR genes are controversial in different ethnic groups. Hopefully, this summary could possibly help researchers and physicians understand the mechanism of T2DM so as to diagnose and even prevent T2DM at early time.

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          IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045

          J.D. da Rocha Fernandes, Y. Huang, J.E. Shaw … (2018)
          Since the year 2000, IDF has been measuring the prevalence of diabetes nationally, regionally and globally.
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            Prevalence and control of diabetes in Chinese adults.

            Yu Xu, Limin Wang, Jiang Ping He … (2013)
            Noncommunicable chronic diseases have become the leading causes of mortality and disease burden worldwide. To investigate the prevalence of diabetes and glycemic control in the Chinese adult population. Using a complex, multistage, probability sampling design, we conducted a cross-sectional survey in a nationally representative sample of 98,658 Chinese adults in 2010. Plasma glucose and hemoglobin A1c levels were measured after at least a 10-hour overnight fast among all study participants, and a 2-hour oral glucose tolerance test was conducted among participants without a self-reported history of diagnosed diabetes. Diabetes and prediabetes were defined according to the 2010 American Diabetes Association criteria; whereas, a hemoglobin A1c level of <7.0% was considered adequate glycemic control. The overall prevalence of diabetes was estimated to be 11.6% (95% CI, 11.3%-11.8%) in the Chinese adult population. The prevalence among men was 12.1% (95% CI, 11.7%-12.5%) and among women was 11.0% (95% CI, 10.7%-11.4%). The prevalence of previously diagnosed diabetes was estimated to be 3.5% (95% CI, 3.4%-3.6%) in the Chinese population: 3.6% (95% CI, 3.4%-3.8%) in men and 3.4% (95% CI, 3.2%-3.5%) in women. The prevalence of undiagnosed diabetes was 8.1% (95% CI, 7.9%-8.3%) in the Chinese population: 8.5% (95% CI, 8.2%-8.8%) in men and 7.7% (95% CI, 7.4%-8.0%) in women. In addition, the prevalence of prediabetes was estimated to be 50.1% (95% CI, 49.7%-50.6%) in Chinese adults: 52.1% (95% CI, 51.5%-52.7%) in men and 48.1% (95% CI, 47.6%-48.7%) in women. The prevalence of diabetes was higher in older age groups, in urban residents, and in persons living in economically developed regions. Among patients with diabetes, only 25.8% (95% CI, 24.9%-26.8%) received treatment for diabetes, and only 39.7% (95% CI, 37.6%-41.8%) of those treated had adequate glycemic control. The estimated prevalence of diabetes among a representative sample of Chinese adults was 11.6% and the prevalence of prediabetes was 50.1%. Projections based on sample weighting suggest this may represent up to 113.9 million Chinese adults with diabetes and 493.4 million with prediabetes. These findings indicate the importance of diabetes as a public health problem in China.
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              New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk

              Josée Dupuis, Claudia Langenberg, Inga Prokopenko … (2010)
              Circulating glucose levels are tightly regulated. To identify novel glycemic loci, we performed meta-analyses of 21 genome-wide associations studies informative for fasting glucose (FG), fasting insulin (FI) and indices of β-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 non-diabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with FG/HOMA-B and two associated with FI/HOMA-IR. These include nine new FG loci (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and FAM148B) and one influencing FI/HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB/TMEM195 with type 2 diabetes (T2D). Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify T2D risk loci, as well as loci that elevate FG modestly, but do not cause overt diabetes.
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                Author and article information

                Contributors
                Cuilin Li:
                ORCID: http://orcid.org/0000-0002-9480-1532
                licuilincindy@163.com
                Journal
                Journal ID (nlm-ta): Diabetol Metab Syndr
                Journal ID (iso-abbrev): Diabetol Metab Syndr
                Title: Diabetology & Metabolic Syndrome
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1758-5996
                Publication date (Electronic): 4 November 2020
                Publication date PMC-release: 4 November 2020
                Publication date Collection: 2020
                Volume: 12
                Electronic Location Identifier: 97
                Affiliations
                [1 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Department of Pharmacy, , The Affiliated Zhuzhou Hospital Xiangya Medical College CSU, ; Zhuzhou, 412007 Hunan China
                [2 ]Laboratory Medical Center, The Affiliated Zhuzhou Hospital Xiangya Medical College CSU, Zhuzhou, 412007 China
                [3 ]Department of Metabolism and Endocrinology, The Affiliated Zhuzhou Hospital Xiangya Medical College CSU, Zhuzhou, 412007 China
                Author information
                http://orcid.org/0000-0002-9480-1532
                Article
                Publisher ID: 604
                DOI: 10.1186/s13098-020-00604-5
                PMC ID: 7643457
                PubMed ID: 33292424
                SO-VID: abb39d39-392a-4565-803f-34d92a84a81a
                Copyright © © The Author(s) 2020
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 29 June 2020
                Date revision received : 22 October 2020
                Date accepted : 26 October 2020
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: type 2 diabetes mellitus,genetic polymorphism,g6pc2,gck,gckr,oct3
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: type 2 diabetes mellitus, genetic polymorphism, g6pc2, gck, gckr, oct3

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