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      Effect of bilirubin concentration on the risk of diabetic complications: A meta-analysis of epidemiologic studies

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      Author(s): a , 1 , 2 , 3 , 4
      Publication date (Electronic):
      Journal: Scientific Reports
      Publisher: Nature Publishing Group

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          Abstract

          Diabetes can affect many parts of the body and is associated with serious complications. Oxidative stress is a major contributor in the pathogenesis of diabetic complications and bilirubin has been shown to have antioxidant effects. The number of studies on the effect of bilirubin on the risk of diabetic complications has increased, but the results are inconsistent. Thus, we performed a meta-analysis to determine the relationship between bilirubin concentration and the risk of diabetic complications, and to investigate if there was a dose-response relationship. We carried out an extensive search in multiple databases. A fixed or random-effects model was used to calculate the pooled estimates. We conducted a dose-response meta-analysis to analyze the association between these estimates. A total of 132,240 subjects from 27 included studies were analyzed in our meta-analysis. A negative nonlinear association between bilirubin concentration and the risk of diabetic complications was identified (OR: 0.77, 95% CI: 0.73–0.81), with a nonlinear association. We also found that there was a negative association between bilirubin concentration and the risk of diabetic nephropathy, diabetic retinopathy and diabetic neuropathy. The results of our meta-analysis indicate that bilirubin may play a protective role in the occurrence of diabetic complications.

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          Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence

          James Boyle, Theodore Thompson, Edward Gregg … (2010)
          Background People with diabetes can suffer from diverse complications that seriously erode quality of life. Diabetes, costing the United States more than $174 billion per year in 2007, is expected to take an increasingly large financial toll in subsequent years. Accurate projections of diabetes burden are essential to policymakers planning for future health care needs and costs. Methods Using data on prediabetes and diabetes prevalence in the United States, forecasted incidence, and current US Census projections of mortality and migration, the authors constructed a series of dynamic models employing systems of difference equations to project the future burden of diabetes among US adults. A three-state model partitions the US population into no diabetes, undiagnosed diabetes, and diagnosed diabetes. A four-state model divides the state of "no diabetes" into high-risk (prediabetes) and low-risk (normal glucose) states. A five-state model incorporates an intervention designed to prevent or delay diabetes in adults at high risk. Results The authors project that annual diagnosed diabetes incidence (new cases) will increase from about 8 cases per 1,000 in 2008 to about 15 in 2050. Assuming low incidence and relatively high diabetes mortality, total diabetes prevalence (diagnosed and undiagnosed cases) is projected to increase from 14% in 2010 to 21% of the US adult population by 2050. However, if recent increases in diabetes incidence continue and diabetes mortality is relatively low, prevalence will increase to 33% by 2050. A middle-ground scenario projects a prevalence of 25% to 28% by 2050. Intervention can reduce, but not eliminate, increases in diabetes prevalence. Conclusions These projected increases are largely attributable to the aging of the US population, increasing numbers of members of higher-risk minority groups in the population, and people with diabetes living longer. Effective strategies will need to be undertaken to moderate the impact of these factors on national diabetes burden. Our analysis suggests that widespread implementation of reasonably effective preventive interventions focused on high-risk subgroups of the population can considerably reduce, but not eliminate, future increases in diabetes prevalence.
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              The Role of Bilirubin in Diabetes, Metabolic Syndrome, and Cardiovascular Diseases

              Libor Vitek (2012)
              Bilirubin belongs to a phylogenetically old superfamily of tetrapyrrolic compounds, which have multiple biological functions. Although for decades bilirubin was believed to be only a waste product of the heme catabolic pathway at best, and a potentially toxic compound at worst; recent data has convincingly demonstrated that mildly elevated serum bilirubin levels are strongly associated with a lower prevalence of oxidative stress-mediated diseases. Indeed, serum bilirubin has been consistently shown to be negatively correlated to cardiovascular diseases (CVD), as well as to CVD-related diseases and risk factors such as arterial hypertension, diabetes mellitus, metabolic syndrome, and obesity. In addition, the clinical data are strongly supported by evidence arising from both in vitro and in vivo experimental studies. This data not only shows the protective effects of bilirubin per se; but additionally, of other products of the heme catabolic pathway such as biliverdin and carbon monoxide, as well as its key enzymes (heme oxygenase and biliverdin reductase); thus, further underlining the biological impacts of this pathway. In this review, detailed information on the experimental and clinical evidence between the heme catabolic pathway and CVD, and those related diseases such as diabetes, metabolic syndrome, and obesity is provided. All of these pathological conditions represent an important threat to human civilization, being the major killers in developed countries, with a steadily increasing prevalence. Thus, it is extremely important to search for novel markers of these diseases, as well as for novel therapeutic modalities to reverse this unfavorable situation. The heme catabolic pathway seems to fulfill the criteria for both diagnostic purposes as well as for potential therapeutical interventions.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 30 January 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 41681
                Affiliations
                [1 ]Department of Cancer Prevention and Treatment, Cancer Hospital of China Medical University/Liaoning Cancer Hospital & Institute Shenyang , People’s Republic of China
                [2 ]Department of Clinical Epidemiology and Evidence Medicine, The First Hospital of China Medical University , Shenyang, People’s Republic of China
                [3 ]Leiden University Center for Linguistics and Leiden Institute for Brain and Congnition , leiden, zuid-holland, Netherlands
                [4 ]Department of mathematics, School of Fundamental Sciences, China Medical University , Shenyang, People’s Republic of China
                Author notes
                Article
                Publisher Item ID: srep41681
                DOI: 10.1038/srep41681
                PMC ID: 5278382
                PubMed ID: 28134328
                SO-VID: 603d7886-5a94-4444-9c48-1f1504a487cb
                Copyright © Copyright © 2017, The Author(s)
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 18 May 2016
                Date accepted : 28 December 2016
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