Type 2 diabetes occurrence and mercury exposure – From the National Nutrition and Health Survey in Taiwan

Tsai, Tsung-Neng; Kuo, Chin‐Chi; Pan, Wen‐Harn; Wu, Trong-Neng; Lin, Pinpin; Wang, Shuli

doi:10.1016/j.envint.2019.02.038

Cited by 26 publications

(16 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, MeHg is related to T2D risk in some but not all epidemiological studies (reviewed in 119 ). Most notably, cross-sectional analyses in the population-representative National Health and Nutrition Examination Surveys (NHANES) in the United States 120 and Taiwan 121 show positive associations between T2D and MeHg exposure. A large prospective human study confirmed this positive association 122 .…”

Section: Discussionmentioning

confidence: 99%

High exposure variance enables candidate biomarker detection in a small EWAS of methylmercury-exposed Peruvian adults

Weinhouse

Perez

Ryde

et al. 2022

Preprint

View full text Add to dashboard Cite

Background: Methylmercury (MeHg) is an environmental pollutant of global public health concern. MeHg is associated with immune dysfunction but the underlying mechanisms are unclear. The most common route of MeHg exposure is through consumption of fatty fish that contain beneficial n-3 polyunsaturated fatty acids (PUFA) that may protect against MeHg toxicity. Objectives: To better inform individual costs and benefits of fish consumption, we aimed to identify candidate epigenetic biomarkers of biological responses that reflect MeHg toxicity and PUFA protection. Methods: We profiled genome-wide DNA methylation using Illumina Infinium MethylationEPIC BeadChip in whole blood from N=32 individuals from Madre de Dios, Peru. Madre de Dios has high artisanal and small-scale gold mining activity, which results in high MeHg exposure to nearby residents. We compared DNA methylation in N=16 individuals with high (>10 μg/g) vs. N=16 individuals with low (<1 μg/g) total hair mercury (a proxy for methylmercury exposure), matched on age and sex. Results: We identified hypomethylated (i.e., likely activated) genes and promoters in high vs. low MeHg-exposed participants linked to Th1/Th2 immune imbalance, decreased IL-7 signaling, and increased marginal zone B cells. These three pathways are feasible mechanisms for MeHg-induced autoimmunity. In addition, we identified candidate epigenetic biomarkers of PUFA-mediated protection: hypomethylated enhancer binding sites for retinoid X receptor (RXR) and retinoic acid receptor α (RARα). Last, we observed hypomethylated enhancer and promoter binding sites for glucocorticoid receptor (GR), which is associated with developmental neurotoxicity, and transcription factor 7-like 2 (TCF7L2), which is associated with type 2 diabetes (T2D) risk. Discussion: Here, we identify a set of candidate epigenetic biomarkers for assessing individualized risk of autoimmune response and protection against neurotoxicity due to MeHg exposure and fish consumption. In addition, our results may inform surrogate tissue biomarkers of early MeHg exposure-related neurotoxicity and T2D risk.

show abstract

Section: Discussionmentioning

confidence: 99%

High exposure variance enables candidate biomarker detection in a small EWAS of methylmercury-exposed Peruvian adults

Weinhouse

Perez

Ryde

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…This link is well understood; according to Houston (2011), "Mercury toxicity should be evaluated in every patient with hypertension." Heavy metals have also been associated with diabetes and obesity [27] , [28] , [29] , [30] , [31] . However, COVID-19 fatalities seem to be associated with the immune system initiating a "cytokine storm," in which abnormally high quantities of cytokines are generated, initiating a cascade of events that might result in death.…”

Section: Introductionmentioning

confidence: 99%

Selenium and mercury concentrations in biological samples from patients with COVID-19

Chanihoon

Afridi

Unar

et al. 2022

Journal of Trace Elements in Medicine and Biology

View full text Add to dashboard Cite

“…12) Number of studies suggested that methylmercury is a risk factor for the neural development of fetus, 13,14) while some recent epidemiological studies suggested that methylmercury could rise risk of diabetes. 15,16) Studies of cultured cells and in vivo have shown that excess methylmercury causes inhibition of insulin secretion in pancreatic β-cells via oxidative stresses and inducing cell death. 17) However, the effects of sub-cytotoxic methylmercury on pancreatic β-cells are not well understood.…”

Section: Introductionmentioning

confidence: 99%

Effects of the Interplay between Selenocystine and Methylmercury on Their Cytotoxicity and Glucose-Driven Insulin Secretion from Mouse Insulinoma Cells

et al. 2022

View full text Add to dashboard Cite

We've previously shown that high levels of selenoprotein P (SeP), a major selenoprotein in plasma, can be a risk factor of type 2 diabetes. It was also thought that inhibition of insulin secretion caused by over-supplementation of selenium by SeP to pancreatic β cells contributed to the progress of diabetes. On the other hand, methylmercury, which is an environmental pollutant, is known to cancel the action of selenium via the covalent modification. Therefore, we thought that the interaction between selenium and methylmercury could be associated with the pathogenesis of diabetes. To address the hypothesis, MIN6 cells, a mouse pancreatic β-cell line, were treated with selenocystine (as a selenium donner) and methylmercury then examined insulin release from the cells. Selenocystine (400-1200 nM), which corresponds to the concentration of selenium in SeP of diabetic patients, shows cytotoxicity and inhibited glucose-driven insulin secretion. Methylmercury rescued the cytotoxicity that induced by selenocystine, however it affected the insulin secretion that is depressed by selenocystine at little intense. These data indicate that the mechanisms underlying inhibition of insulin secretion by selenocystine are independent of cytotoxicity, and methylmercury cannot be expected to restore insulin secretion or suppress diabetes as selenium neutlizer.

show abstract

Type 2 diabetes occurrence and mercury exposure – From the National Nutrition and Health Survey in Taiwan

Cited by 26 publications

References 53 publications

High exposure variance enables candidate biomarker detection in a small EWAS of methylmercury-exposed Peruvian adults

High exposure variance enables candidate biomarker detection in a small EWAS of methylmercury-exposed Peruvian adults

Selenium and mercury concentrations in biological samples from patients with COVID-19

Effects of the Interplay between Selenocystine and Methylmercury on Their Cytotoxicity and Glucose-Driven Insulin Secretion from Mouse Insulinoma Cells

Contact Info

Product

Resources

About