Abstract
Brominated flame retardants exposure has been associated with increasing trends of diabetes and metabolic disease. Thus, the purpose of this study was to provide evidence of polybrominated diphenyl ethers (PBDEs) exposure in relation to diabetes prevalence and to reveal the potential underlying mechanism in epidemiological and animal studies. All the participants received a questionnaire, health examination, and the detection of 7 PBDE congeners in serum in two independent community-based studies from 2011 to 2012 in China. Male rats were exposed to 2,2’4,4’-tetrabromodiphenyl ether (BDE47) for 8 weeks to explore its effects on glucose homeostasis and potential mechanisms using high-throughput genomic analysis. Among the 7 congeners, BDE47 showed significant high detection rate and concentration in cases in Study I and Study II. Every tertile of BDE47 exposure significantly increased the risk of diabetes prevalence in Study I (Ptrend = 0.001) and Study II (Ptrend < 0.001). Additionally, BDE47 treatments induced hyperglycemia in rats. Furthermore, gene microarray analysis showed that diabetes pathway and three gene ontology terms involved in glucose transport were enriched. The results indicated that environmental exposure to BDE47 was associated with increased diabetes prevalence. However, further prospective and mechanistic studies are needed to the causation of diabetes in relation to BDE47.
Highlights
Characteristics Current smoking Current drinking Family history of hypertension Family history of diabetes Hypertension Hypercholesterolemia Hypertriglyceridemia high density lipoprotein cholesterol (HDLC) < 1.40 mmol/L low density lipoprotein cholesterol (LDLC) > 4.14 mmol/L Dyslipidemia Central obesity Obesity alanine transarninase (ALT) > 40 U/L AST > 40 U/L blood urea nitrogen (BUN) > 7.14 mmol/L Hyperuricemia CREA > 133 μmol/L
Our study firstly explored the potential relationship between the exposure to BDE47 and diabetes development using both epidemiological and experimental strategies
Results from the pairwise case-control study demonstrated that environmental exposure to BDE47 was positively associated with human diabetes prevalence, which was strengthened by the animal experiment results showing that BDE47 could significantly increase high fasting glucose in rats and enrich T1D pathways with the involvement of some related genes, such as Tnf, Ins[2], Adipoq, and Ednra
Summary
Characteristics Current smoking Current drinking Family history of hypertension Family history of diabetes Hypertension Hypercholesterolemia Hypertriglyceridemia HDLC < 1.40 mmol/L LDLC > 4.14 mmol/L Dyslipidemia Central obesity Obesity ALT > 40 U/L AST > 40 U/L BUN > 7.14 mmol/L Hyperuricemia CREA > 133 μmol/L. Accumulating epidemiological evidence has demonstrated that exposure to PBDEs might be potentially associated with the risk of diabetes[12]. In previous human studies, including male and female, BDE47 tended to be positively associated with the prevalence of diabetes, but did not reach statistical significance[14,16]. The purpose of the study was to provide epidemiological evidence of the association between environmental exposure to PBDEs and diabetes, and try to reveal the specific underlying mechanism in an animal model. In study I, we explored the relationship between PBDEs exposure and diabetes using a 245 paired case-control, which was validated further using an independent 565 paired case-control in study II. We examined the effects of BDE47 on the onset of diabetes in animals, and conducted the potential mechanism using gene microarray and related bioinformatics analysis. The present study will be helpful to provide better understanding of PBDEs in relation to diabetes
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