For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
2
views
34
references
 Top references
cited by
5
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      185
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Association Between Serum Albumin Levels and Diabetic Peripheral Neuropathy Among Patients with Type 2 Diabetes: Effect Modification of Body Mass Index

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          The role of serum albumin in the risk of diabetic peripheral neuropathy (DPN) remains unclear. This study aimed to explore the relationship between serum albumin level and DPN, and to examine any possible effect modifiers among patients with type 2 diabetes mellitus.

          Methods

          This cross-sectional study was conducted in Jiangxi, China, from May 2012 to December 2014. Serum albumin levels were determined in 523 subjects, and the association between serum albumin level and DPN was evaluated using linear regression models (odds ratio [OR] and corresponding 95% confidence interval [CI]).

          Results

          There was a significant inverse association between serum albumin level (per 1 g/L increment, OR 0.95 [95% CI 0.92–0.98]) and the risk of DPN. Accordingly, when serum albumin was assessed as quartiles, a significantly lower risk of DPN was found in participants in quartile 4 (OR 0.49 [95% CI 0.25–0.95]), compared with those in quartile 1. Consistently, higher albumin levels (≥35 g/L) were associated with decreased odds for DPN (OR 0.36 [95% CI 0.17–0.74]) compared with lower levels. Furthermore, the albumin–DPN association was significantly stronger in patients with a relatively high body mass index (BMI; ≥24 kg/m 2; OR 0.91 [95% CI 0.85–0.98]) than in those with a low BMI (<24 kg/m 2; OR 0.99 [95% CI 0.94–1.04]; P for interaction = 0.042).

          Conclusion

          These data suggest that serum albumin level could be a novel risk factor for DPN among patients with type 2 diabetes and relatively high BMI (>24 kg/m 2).

          Related collections

          Most cited references34

          • Record: found
          • Abstract: found
          • Article: not found

          Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation.

          K.G.M.M. Alberti, P.Z. Zimmet (1998)
          The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
          Article 0 comments Cited 1170 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Oxidative stress and diabetic complications.

            Ferdinando Giacco, Michael Brownlee, Ann Marie Schmidt (2010)
            Oxidative stress plays a pivotal role in the development of diabetes complications, both microvascular and cardiovascular. The metabolic abnormalities of diabetes cause mitochondrial superoxide overproduction in endothelial cells of both large and small vessels, as well as in the myocardium. This increased superoxide production causes the activation of 5 major pathways involved in the pathogenesis of complications: polyol pathway flux, increased formation of AGEs (advanced glycation end products), increased expression of the receptor for AGEs and its activating ligands, activation of protein kinase C isoforms, and overactivity of the hexosamine pathway. It also directly inactivates 2 critical antiatherosclerotic enzymes, endothelial nitric oxide synthase and prostacyclin synthase. Through these pathways, increased intracellular reactive oxygen species (ROS) cause defective angiogenesis in response to ischemia, activate a number of proinflammatory pathways, and cause long-lasting epigenetic changes that drive persistent expression of proinflammatory genes after glycemia is normalized ("hyperglycemic memory"). Atherosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS. Overexpression of superoxide dismutase in transgenic diabetic mice prevents diabetic retinopathy, nephropathy, and cardiomyopathy. The aim of this review is to highlight advances in understanding the role of metabolite-generated ROS in the development of diabetic complications.
            Article 0 comments Cited 726 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Biochemistry and molecular cell biology of diabetic complications.

              M. Brownlee (2001)
              Diabetes-specific microvascular disease is a leading cause of blindness, renal failure and nerve damage, and diabetes-accelerated atherosclerosis leads to increased risk of myocardial infarction, stroke and limb amputation. Four main molecular mechanisms have been implicated in glucose-mediated vascular damage. All seem to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain. This integrating paradigm provides a new conceptual framework for future research and drug discovery.
              Article 0 comments Cited 636 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Diabetes Metab Syndr Obes
                Journal ID (iso-abbrev): Diabetes Metab Syndr Obes
                Journal ID (publisher-id): dmso
                Title: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
                Publisher: Dove
                ISSN (Electronic): 1178-7007
                Publication date (Electronic): 22 February 2022
                Publication date Collection: 2022
                Volume: 15
                Pages: 527-534
                Affiliations
                [1 ]Department of Endocrinology and Metabolism, First Affiliated Hospital of Nanchang University , Nanchang, Jiangxi, 330006, People’s Republic of China
                [2 ]Jiangxi Clinical Research Center for Endocrine and Metabolic Disease , Nanchang, Jiangxi, 330006, People's Republic of China
                [3 ]Jiangxi Branch of National Clinical Research Center for Metabolic Disease , Nanchang, JIangxi, 330006, People's Republic of China
                Author notes
                Correspondence: Jixiong Xu; Jiancheng Wang, Department of Endocrinology and Metabolism, First Affiliated Hospital of Nanchang University , No. 17, Yongwaizheng Street, Nanchang, Jiangxi, 330006, People’s Republic of China, Tel/Fax +86-791-86836960, Email Jixiong.Xu@ncu.edu.cn; jasonwong2015@163.com
                Article
                Publisher ID: 347349
                DOI: 10.2147/DMSO.S347349
                PMC ID: 8881928
                PubMed ID: 35228809
                SO-VID: 7b508a1b-6d95-48ec-b0d6-8c7f6c42c169
                Copyright © © 2022 Hu et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 02 November 2021
                Date accepted : 18 January 2022
                Page count
                Figures: 2, Tables: 8, References: 34, Pages: 8
                Funding
                Funded by: the National Natural Science Funds of China;
                Funded by: the National Natural Science Funds of Jiangxi Province;
                The study was supported by funding from the following: the National Natural Science Funds of China (Nos. 81760168 and 81460018) and the National Natural Science Funds of Jiangxi Province (No. 20192BAB205031).
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: serum albumin,bmi,diabetic peripheral neuropathy,type 2 diabetes mellitus
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: serum albumin, bmi, diabetic peripheral neuropathy, type 2 diabetes mellitus

                Comments

                Comment on this article

                scite_

                Similar content185

                See all similar

                Cited by5

                See all cited by

                Most referenced authors379

                See all reference authors