US EPA

3861018 

Journal Article 

Persistent Organic Pollutants Impair Insulin Secretory Function of Pancreatic Beta-Cells: Human and in Vitro Evidence 

Lee, YM; Ha, CM; Kim, SA; Thoudam, T; Yoon, YR; Kim, DJ; Kim, HC; Moon, HB; Park, S; Lee, IK; Lee, DH 

2017 

Yes 

Diabetes
ISSN: 0012-1797
EISSN: 1939-327X 

66 

10 

2669-2680 

English 

28720696 

10.2337/db17-0188 

WOS:000411195800014 

Persistent organic pollutants (POPs), especially organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs), have emerged as a new risk factor of type 2 diabetes (T2D). We evaluated whether chronic exposure to low-dose POPs affects insulin secretory function of beta-cells in humans and in vitro cells. Serum concentrations of OCPs and PCBs were measured in 200 nondiabetic adults. Mathematical-model-based insulin secretion indices were estimated using a 2-hour 7-sample oral glucose tolerance test. Insulin secretion by INS1E beta-cells was measured after 48-hour treatment with 3 OCPs or a PCB mixture. Static second-phase insulin secretion significantly decreased with increasing serum concentrations of OCPs. Adjusted means were 63.2, 39.3, 44.1, 39.3, 39.7, and 22.3 across six categories of a summary measure of OCPs (Ptrend = 0.02). Dynamic first-phase insulin secretion remarkably decreased only among insulin-sensitive individuals with increasing concentrations of OCPs (Ptrend = 0.02); the insulin levels among subjects with high OCPs were about 30% of those with low OCPs. Compared to OCPs, PCBs showed weaker associations. The decreased insulin secretion by INS1E beta-cells was observed for even 1 pM OCPs. Our data from human subjects and in vitro cell experiments suggest that chronic exposure to low-dose POPs, especially OCPs, can induce pancreatic beta-cell dysfunction.