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      Blood Mercury and Insulin Resistance in Nondiabetic Koreans (KNHANES 2008-2010)

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          Abstract

          Purpose

          Blood mercury levels are associated with inflammation, and chronic low-grade inflammation is a cause of insulin resistance. This study aimed to investigate the association between serum mercury and insulin resistance.

          Materials and Methods

          Subjects from the 2008-2010 Korean National Health and Nutrition Examination Survey were selected (n=29235) and the relevant data of 5388 subjects (2643 males and 2745 females) were analyzed cross-sectionally. Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) was compared according to blood mercury quartiles, and the odds ratio (OR) of having the highest quartile of HOMA-IR according to blood mercury quartiles was calculated.

          Results

          Blood mercury levels in men and women were 29.4 nmol/L and 20.5 nmol/L, respectively, and fasting blood sugar (FBS), insulin, and HOMA-IR were significantly correlated with blood mercury levels. The correlation was stronger in men than in women. In men, FBS and HOMA-IR showed step-wise increases as the quartiles of blood mercury increased; only HOMA-IR differed significantly in the third and fourth blood mercury quartiles, compared to the first quartile. In women, however, both FBS and HOMA-IR differed significantly in the third and fourth blood mercury quartiles, compared to the first quartile. Among men, the OR of being in the highest HOMA-IR quartile was greatest for the highest blood mercury quartile (OR=1.720, 95% CI; 1.172-2.526), compared with the lowest quartile.

          Conclusion

          In this large population-based study, blood mercury levels were weakly correlated with HOMA-IR and may be a risk factor for insulin resistance in nondiabetic Koreans.

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          Metabolic syndrome, insulin resistance, and roles of inflammation--mechanisms and therapeutic targets.

          Giulio Romeo, Jongsoon Lee, Steven Shoelson (2012)
          Obesity and its comorbidities, including type 2 diabetes mellitus and cardiovascular disease, are associated with a state of chronic low-grade inflammation that can be detected both systemically and within specific tissues. Areas of active investigation focus on the molecular bases of metabolic inflammation and potential pathogenic roles in insulin resistance, diabetes, and cardiovascular disease. An increased accumulation of macrophages occurring in obese adipose tissue has emerged as a key process in metabolic inflammation. Recent studies have also begun to unravel the heterogeneity of adipose tissue macrophages, and their physical and functional interactions with adipocytes, endothelial cells, and other immune cells within the adipose tissue microenvironment. Translating the information gathered from experimental models of insulin resistance and diabetes into meaningful therapeutic interventions is a tantalizing goal with long-term global health implications. In this context, ongoing clinical studies are testing the effects of targeting inflammation systemically on metabolic and cardiovascular outcomes.
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            Prevalence and determinants of insulin resistance among U.S. adolescents: a population-based study.

            Megumi Okumura, William Herman, Mi-Hwa Lee … (2006)
            We sought to examine the distribution of insulin and homeostasis model assessment of insulin resistance (HOMA-IR) and associations of HOMA-IR with sex, race/ethnicity, age, and weight status, as measured by BMI, among U.S. adolescents. Of 4,902 adolescents aged 12-19 years who participated in the National Health and Nutrition Examination Survey 1999-2002, analysis was performed for a nationally representative subsample of 1,802 adolescents without diabetes who had fasting laboratory measurements. The main outcome measure was HOMA-IR, calculated from fasting insulin and glucose and log transformed for multiple linear regression analyses. In adjusted regression models that included age and weight status, girls had higher HOMA-IR than boys and Mexican-American children had higher HOMA-IR levels than white children. There were no significant differences in adjusted HOMA-IR between black and white children. Obese children (BMI >/=95th percentile) had significantly higher levels of HOMA-IR compared with children of normal weight (BMI <85th percentile) in adjusted comparisons (mean HOMA-IR 4.93 [95% CI 4.56-5.35] vs. 2.30 [2.21-2.39], respectively). Weight status was by far the most important determinant of insulin resistance, accounting for 29.1% of the variance in HOMA-IR. The prevalence of insulin resistance in obese adolescents was 52.1% (95% CI 44.5-59.8). Obesity in U.S. adolescents represents the most important risk factor for insulin resistance, independent of sex, age, or race/ethnicity. The prevalence of insulin resistance in obese children foreshadows a worrisome trend for the burden of type 2 diabetes in the U.S.
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              Impact of insulin resistance on risk of type 2 diabetes and cardiovascular disease in people with metabolic syndrome.

              James Meigs, Martin K. Rutter, Lisa M. Sullivan … (2007)
              Metabolic syndrome increases the risk for type 2 diabetes and cardiovascular disease (CVD) and may be associated with insulin resistance. We tested the hypothesis that the metabolic syndrome confers risk with or without concomitant insulin resistance among 2,803 Framingham Offspring Study subjects followed up to 11 years for new diabetes (135 cases) or CVD (240 cases). We classified subjects by presence of metabolic syndrome (using the National Cholesterol Education Program's [NCEPs] Third Adult Treatment Panel [ATP III], International Diabetes Federation [IDF], or European Group for the Study of Insulin Resistance [EGIR] criteria) and insulin resistance (homeostasis model assessment of insulin resistance > or = 75th percentile) and used separate risk factor-adjusted proportional hazards models to estimate relative risks (RRs) for diabetes or CVD using as referents those without insulin resistance, metabolic syndrome, or without both. Fifty-six percent of individuals with ATP III, 52% with IDF, and 100% with EGIR definitions of metabolic syndrome had insulin resistance. Insulin resistance increased risk for diabetes (RR 2.6 [95% CI 1.7-4.0]) and CVD (1.8 [1.4-2.3]) as did metabolic syndrome for diabetes (ATP III, 3.5 [2.2-5.6]; IDF, 4.6 [2.7-7.7]; and EGIR, 3.3 [2.1-5.1]) and CVD (ATP III, 1.8 [1.4-2.3]; IDF, 1.7 [1.3-2.3]; and EGIR, 2.1 [1.6-2.7]). Relative to those without either metabolic syndrome or insulin resistance, metabolic syndrome and insulin resistance increased risk for diabetes (ATP III, 6.0 [3.3-10.8] and IDF, 6.9 [3.7-13.0]) and CVD (ATP III, 2.3 [1.7-3.1] and IDF, 2.2 [1.6-3.0]). Any instance of metabolic syndrome without insulin resistance increased risk for diabetes approximately threefold (P < 0.001); IDF metabolic syndrome without insulin resistance (RR 1.6, P = 0.01), but not ATP III metabolic syndrome without insulin resistance (RR 1.3, P = 0.2), increased risk for CVD. Metabolic syndrome increased risk for diabetes regardless of insulin resistance. Metabolic syndrome by ATP III criteria may require insulin resistance to increase risk for CVD. The simultaneous presence of metabolic syndrome and insulin resistance identifies an especially high-risk individual.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Yonsei Med J
                Journal ID (iso-abbrev): Yonsei Med. J
                Journal ID (publisher-id): YMJ
                Title: Yonsei Medical Journal
                Publisher: Yonsei University College of Medicine
                ISSN (Print): 0513-5796
                ISSN (Electronic): 1976-2437
                Publication date (Print): 01 July 2015
                Publication date (Electronic): 05 June 2015
                Volume: 56
                Issue: 4
                Pages: 944-950
                Affiliations
                [1 ]Department of Family Practice and Community Health, Ajou University School of Medicine, Suwon, Korea.
                [2 ]CHA Antiaging Institute, CHA University, Seoul, Korea.
                Author notes
                Corresponding author: Dr. Nam-Seok Joo, Department of Family Practice and Community Health, Ajou University School of Medicine, 164 World cup-ro, Yeongtong-gu, Suwon 443-380, Korea. Tel: 82-31-219-5324, Fax: 82-31-219-5218, jchcmc@ 123456hanmail.net
                Article
                DOI: 10.3349/ymj.2015.56.4.944
                PMC ID: 4479861
                PubMed ID: 26069115
                SO-VID: 7521494b-20c1-4de6-a7b2-a9d302044fca
                Copyright © © Copyright: Yonsei University College of Medicine 2015
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 February 2014
                Date revision received : 23 July 2014
                Date accepted : 01 September 2014
                Funding
                Funded by: Rural Development Administration
                Award ID: PJ010059
                Categories
                Subject: Original Article
                Subject: Endocrinology & Metabolism

                ScienceOpen disciplines: Medicine
                Keywords: mercury,insulin resistance,environment,inflammation,korean
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: mercury, insulin resistance, environment, inflammation, korean

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