Exposure to persistent organic pollutants as potential risk factors for developing diabetes

被引:14
作者
Wang ChunXiang
Xu ShunQing [1 ]
Lv ZiQuan
Li YuanYuan
Wang YouJie
Chen Tian
机构
[1] Huazhong Univ Sci & Technol, Key Lab Environm & Hlth, Minist Educ, Wuhan 430030, Peoples R China
基金
中国国家自然科学基金;
关键词
persistent organic pollutants; diabetes; dioxins; polychlorinated biphenyls; organochlorine pesticides; POLYBROMINATED DIPHENYL ETHERS; HUMAN ADIPOSE-TISSUE; GROWTH-FACTOR-I; NUTRITION EXAMINATION SURVEY; TUMOR-NECROSIS-FACTOR; AIR-FORCE VETERANS; POLYCHLORINATED-BIPHENYLS; BISPHENOL-A; ORGANOCHLORINE PESTICIDES; SERUM CONCENTRATIONS;
D O I
10.1007/s11426-010-0157-1
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Persistent organic pollutants (POPs), such as dioxins, polychlorinated biphenyls (PCBs), and organochlorine pesticides (OCPs), which are synthetic chemicals or by-products with an intrinsic resistance to natural degradation processes, are released into the environment, resulting in the widespread dispersal and accumulation in the environment, as well as in human and ecological food chains. Due to their ubiquity in the environment and lipophilic properties, there is emerging concern over the potential risks of human exposure to POPs. Extensive growing evidence indicated that exposure to POPs might be strongly associated with increased risk of a worldwide epidemic of diabetes, especially type 2 diabetes, suggesting that POPs might play a key role in their pathogenesis. Based on summary of the related studies, this paper reviews the epidemiologic and experimental data that addresses the association between increased risk of diabetes and POP exposure, including dioxins, PCBs, OCPs, polybrominated flame retardants (PBFRs), and some environmental estrogens. The potential mechanisms whereby POPs cause diabetes were discussed, such as alterations in lipid metabolism, in glucose transport, in insulin signaling pathway, in steroid metabolism, and disruption of endocrine system, induction of tumor necrosis factor-alpha (TNF-alpha). However, with respect to diabetes, some of the evidence on POPs linked to risk of diabetes was suggestive of a direct or indirect association but was limited or inconclusive. Future research is urgently needed for determining the relative contribution of POPs to diabetes and elucidating the exact mechanisms.
引用
收藏
页码:980 / 994
页数:15
相关论文
共 137 条
[81]   Obesity, metabolic syndrome, and type 2 diabetes: emerging epidemics and their cardiovascular implications [J].
Mensah, GA ;
Mokdad, AH ;
Ford, E ;
Narayan, KMV ;
Giles, WH ;
Vinicor, F ;
Deedwania, PC .
CARDIOLOGY CLINICS, 2004, 22 (04) :485-504
[82]   Diabetes mellitus and 2,3,7,8-tetrachlorodibenzo-p-dioxin elimination in veterans of operation ranch hand [J].
Michalek, JE ;
Ketchum, NS ;
Tripathi, RC .
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, 2003, 66 (03) :211-221
[83]   Serum dioxin, insulin, fasting glucose, and sex hormone-binding globulin in veterans of operation ranch hand [J].
Michalek, JE ;
Akhtar, FZ ;
Kiel, JL .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1999, 84 (05) :1540-1543
[84]   Tissue-specific ablation of the GLUT4 glucose transporter or the insulin receptor challenges assumptions about insulin action and glucose homeostasis [J].
Minokoshi, Y ;
Kahn, CR ;
Kahn, BB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (36) :33609-33612
[85]   MORBIDITY AND MORTALITY IN WORKERS OCCUPATIONALLY EXPOSED TO PESTICIDES [J].
MORGAN, DP ;
LIN, LI ;
SAIKALY, HH .
ARCHIVES OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY, 1980, 9 (03) :349-382
[86]   White adipose tissue:: Storage and effector site for environmental pollutants [J].
Muellerova, D. ;
Kopecky, J. .
PHYSIOLOGICAL RESEARCH, 2007, 56 (04) :375-381
[87]   Concentrations of environmental chemicals associated with neurodevelopmental effects in US population [J].
Needham, LL ;
Barr, DB ;
Caudill, SP ;
Pirkle, JL ;
Turner, WE ;
Osterloh, J ;
Jones, RL ;
Sampson, EJ .
NEUROTOXICOLOGY, 2005, 26 (04) :531-545
[88]  
Nishizumi Masahiro, 1995, Fukuoka Acta Medica, V86, P241
[89]  
NOMEIR AA, 1987, REV ENVIRON CONTAM T, V100, P1
[90]   2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced impairment of glucose-stimulated insulin secretion in isolated rat pancreatic islets [J].
Novelli, M ;
Piaggi, S ;
De Tata, V .
TOXICOLOGY LETTERS, 2005, 156 (02) :307-314