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      Oxidative Stress and Insulin Resistance : The Coronary Artery Risk Development in Young Adults study

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          Abstract

          OBJECTIVE

          Although cumulative evidence suggests that increased oxidative stress may lead to insulin resistance in vivo or in vitro, community-based studies are scarce. This study examined the longitudinal relationships of oxidative stress biomarkers with the development of insulin resistance and whether these relationships were independent of obesity in nondiabetic young adults.

          RESEARCH DESIGN AND METHODS

          Biomarkers of oxidative stress (F 2-isoprostanes [F 2Isop] and oxidized LDL [oxLDL]), insulin resistance (the homeostasis model assessment of insulin resistance [HOMA-IR]), and various fatness measures (BMI, waist circumference, and estimated percent fat) were obtained in a population-based observational study (Coronary Artery Risk Development in Young Adults) and its ancillary study (Young Adult Longitudinal Trends in Antioxidants) during 2000–2006.

          RESULTS

          There were substantial increases in estimated mean HOMA-IR over time. OxLDL and F 2Isop showed little association with each other. Mean evolving HOMA-IR increased with increasing levels of oxidative stress markers ( P < 0.001 for oxLDL and P = 0.06 for F 2Isop), measured in 2000–2001. After additional adjustment for adiposity, a positive association between oxLDL and HOMA-IR was strongly evident, whereas the association between F 2Isop and HOMA-IR was not.

          CONCLUSIONS

          We observed positive associations between each of two oxidative stress markers and insulin resistance. The association with oxidized LDL was independent of obesity, but that with F 2Isop was not.

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          The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes.

          S E Kahn (2003)
          The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes have been debated extensively. The concept that a feedback loop governs the interaction of the insulin-sensitive tissues and the beta cell as well as the elucidation of the hyperbolic relationship between insulin sensitivity and insulin secretion explains why insulin-resistant subjects exhibit markedly increased insulin responses while those who are insulin-sensitive have low responses. Consideration of this hyperbolic relationship has helped identify the critical role of beta-cell dysfunction in the development of Type 2 diabetes and the demonstration of reduced beta-cell function in high risk subjects. Furthermore, assessments in a number of ethnic groups emphasise that beta-cell function is a major determinant of oral glucose tolerance in subjects with normal and reduced glucose tolerance and that in all populations the progression from normal to impaired glucose tolerance and subsequently to Type 2 diabetes is associated with declining insulin sensitivity and beta-cell function. The genetic and molecular basis for these reductions in insulin sensitivity and beta-cell function are not fully understood but it does seem that body-fat distribution and especially intra-abdominal fat are major determinants of insulin resistance while reductions in beta-cell mass contribute to beta-cell dysfunction. Based on our greater understanding of the relative roles of insulin resistance and beta-cell dysfunction in Type 2 diabetes, we can anticipate advances in the identification of genes contributing to the development of the disease as well as approaches to the treatment and prevention of Type 2 diabetes.
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            Body fat assessed from total body density and its estimation from skinfold thickness: measurements on 481 men and women aged from 16 to 72 years.

            J V Durnin, J. Womersley (1974)
            Article 0 comments Cited 305 times – based on 0 reviews     Review now
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              Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study.

              B Martin, J H Warram, A S Krolewski … (1992)
              Type 2 diabetes mellitus is characterised by resistance of peripheral tissues to insulin and a relative deficiency of insulin secretion. To find out which is the earliest or primary determinant of disease, we used a minimum model of glucose disposal and insulin secretion based on intravenous glucose tolerance tests to estimate insulin sensitivity (SI), glucose effectiveness (ie, insulin-independent glucose removal rate, SG), and first-phase and second-phase beta-cell responsiveness in normoglycaemic offspring of couples who both had type 2 diabetes. 155 subjects from 86 families were followed-up for 6-25 years. More than 10 years before the development of diabetes, subjects who developed the disease had lower values of both SI (mean 3.2 [SD 2.4] vs 8.1 [6.7] 10(-3) I min-1 pmol-1 insulin; p < 0.0001) and SG (1.6 [0.9] vs 2.3 [1.2] 10(-2) min-1, p < 0.0001) than did those who remained normoglycaemic). For the subjects with both SI and SG below the group median, the cumulative incidence of type 2 diabetes during the 25 years was 76% (95% confidence interval 54-99). By contrast, no subject with both SI and SG above the median developed the disease. Subjects with low SI/high SG or high SI/low SG had intermediate risks. Insulin secretion, especially first phase, tended to be increased rather than decreased in this prediabetic phase and was appropriate for the level of insulin resistance. The development of type 2 diabetes is preceded by and predicted by defects in both insulin-dependent and insulin-independent glucose uptake; the defects are detectable when the patients are normoglycaemic and in most cases more than a decade before diagnosis of disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Diabetes Care
                Journal ID (hwp): diacare
                Journal ID (pmc): dcare
                Journal ID (publisher-id): Diabetes Care
                Title: Diabetes Care
                Publisher: American Diabetes Association
                ISSN (Print): 0149-5992
                ISSN (Electronic): 1935-5548
                Publication date (Print): July 2009
                Publication date (Electronic): 23 April 2009
                Volume: 32
                Issue: 7
                Pages: 1302-1307
                Affiliations
                [1] 1Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota;
                [2] 2Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota;
                [3] 3Department of Preventive Medicine, School of Medicine, College of Medicine, Kyungpook National University, Daegu, Korea;
                [4] 4Atherosclerosis and Metabolism Unit, Katholieke Universiteit Leuven, Leuven, Belgium;
                [5] 5Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
                [6] 6Department of Nutrition, University of Oslo, Oslo, Norway.
                Author notes
                Corresponding author: David R. Jacobs, jacobs@ 123456epi.umn.edu .
                Article
                Publisher ID: 0259
                DOI: 10.2337/dc09-0259
                PMC ID: 2699736
                PubMed ID: 19389821
                SO-VID: 6e403182-3dac-47ca-9ae4-8578d3b15424
                Copyright © © 2009 by the American Diabetes Association.
                License:

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                Date received : 10 February 2009
                Date accepted : 10 April 2009
                Funding
                Funded by: National Institutes of Health
                Award ID: N01-HC-95095
                Award ID: N01-HC-48047
                Award ID: N01-HC-48048
                Award ID: N01-HC-48049
                Award ID: N01-HC-48050
                Award ID: R01-HL-53560
                Categories
                Subject: Original Research
                Subject: Cardiovascular and Metabolic Risk

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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