Association of blood manganese level with diabetes and renal dysfunction: a cross-sectional study of the Korean general population

Abstract

BackgroundThe purpose of this study was to evaluate the association between blood manganese levels and the prevalence of chronic diseases in the Korean population.MethodsThis was a cross-sectional study based on the Korean National Health and Nutrition Examination Survey (KNAHNES). The study included 3996 participants 20 years of age or older whose blood manganese levels had been measured. The participants were also evaluated for the presence of five chronic diseases: diabetes, renal dysfunction, hypertension, ischemic heart disease, and stroke.ResultsBlood manganese levels were significantly lower in the diabetes group compared with the non-diabetes group (1.26 ± 0.02 vs. 1.35 ± 0.01 μg/dL; p = 0.001) and the renal dysfunction group compared with those with normal renal function (1.28 ± 0.03 vs. 1.35 ± 0.01 μg/dL; p = 0.04). There was no significant association between blood manganese levels and the presence of ischemic heart disease or stroke. A multivariate logistic regression analysis adjusted for age, sex, and body mass index was performed; the odds ratio was 0.652 (95% CI: 0.46–0.92) for diabetes and 0.589 (95% CI: 0.39–0.88) for renal dysfunction when comparing the higher quartiles (Q2-4) with the lowest quartile (Q1) of blood manganese level. The prevalence of diabetes was 7.6% in Q1 and 5.3% in Q2-4 (p = 0.02). Similarly, the prevalence of renal dysfunction was 6.8% in Q1, compared with 4.6% in Q2-4 (p = 0.02).ConclusionThe prevalence of diabetes and renal dysfunction increased in participants with low blood manganese levels, suggesting that blood manganese may play a role in glucose homeostasis and renal function.

Synergic effect of GSTP1 and blood manganese concentrations in Autism Spectrum Disorder

“…Chronic Mn accumulation in the mitochondria has been shown to affect MnSOD activity and could result in an abnormal response to the mechanism that blocks oxidative stress in the mitochondria and protects against endothelial dysfunction (Koh et al, 2014). However, presence or absence of properly functioning GST genes may influence the occurrence of oxidative stress, and subsequently influence the occurrence of mitochondrial damage, decrease effectiveness of antioxidants, and increase susceptibility to neurological and muscular diseases (Pagano et al, 2014).…”

“…Some studies have identified increased blood managese concentrations as a possible factor associated with oxidative stress (Erikson, Dobson, Dorman, & Aschner, 2004; Fernsebner, Zorn, Kanawati, Walker, & Michalke, 2014; Wu et al, 2010). On the other hand, Mn is an essential cofactor for metalloenzyme superoxide dismutase, which protects cells against antioxidant processes (Hope et al, 2006; Koh et al, 2014; Rucker, Thadhani, & Tonelli, 2010). Cells are also protected from oxidative stress by intracellular antioxidants like glutathione along with antioxidant enzymes like manganese superoxide dismutase (MnSOD) (Tamai et al, 2011).…”

“…Some studies reported that dietary Mn does not appear to markedly alter circulating Mn levels or expression of leucocyte MnSOD (Hope et al, 2006). On the other hand, chronic Mn accumulation in the mitochondria appears to affect MnSOD activity, resulting in increased oxidative stress in the mitochondria (Koh et al, 2014). Glutathione S-transferase (GST) genes, including glutathione S-transferase pi ( GSTP1 ), glutathione S-transferase mu 1 ( GSTM1 ), and glutathione S-transferase theta 1 ( GSTT1 ), encode enzymes that can protect cells from oxidative stress; polymorphisms in these genes may influence enzymatic activity (Hayes & Strange, 1995).…”

U-Shaped Association between Plasma Manganese Levels and Type 2 Diabetes

“…Consistent with the aforementioned findings, manganese supplementation enhanced MnSOD activity and protected against T2D and diabetes complications (Burlet and Jain 2013; Lee et al 2013). However, with limited sample populations, several epidemiologic studies have yielded inconsistent associations between manganese levels and T2D (Kazi et al 2008; Koh et al 2014; Rambousková et al 2013). As a transition metal, manganese itself is an oxidant at high concentrations, and it appears to be involved in oxidative damage and mitochondrial dysfunction, which have been implicated in the development of T2D (Lowell and Shulman 2005; Maechler and Wollheim 2001).…”

Manganese and Parenteral Nutrition

“…23 Additional disease states hypothesized to play a role in Mn metabolism include renal dysfunction, diabetes, and metabolic syndrome. 37,38 However, these associations are less well documented and their modifying effects on parenteral nutrition Mn requirements or on the potential adverse effects of Mn are unclear.…”