Metabolism disrupting chemicals and metabolic disorders

被引:748
作者
Heindel, Jerrold J. [1 ]
Blumberg, Bruce [2 ]
Cave, Mathew [3 ]
Machtinger, Ronit [4 ,5 ]
Mantovani, Alberto [6 ]
Mendez, Michelle A. [7 ]
Nadal, Angel [8 ,9 ]
Palanza, Paola [10 ]
Panzica, Giancarlo [11 ,12 ]
Sargis, Robert [13 ]
Vandenberg, Laura N. [14 ]
Saal, Frederick Vom [15 ]
机构
[1] NIEHS, Div Extramural Res & Training, 12233 TW Alexander Dr, Res Triangle Pk, NC 27709 USA
[2] Univ Calif Irvine, Dept Dev & Cell Biol, Irvine, CA USA
[3] Univ Louisville, Div Gastroenterol Hepatol & Nutr, Louisville, KY 40292 USA
[4] Sheba Med Ctr, Tel Aviv, Israel
[5] Tel Aviv Univ, Tel Aviv, Israel
[6] Inst Super St, Rome, Italy
[7] Univ North Carolina Chapel Hill, Sch Publ Hlth, Chapel Hill, NC USA
[8] Miguel Hernandez Univ Elche, Inst Bioengn, Alicante, Spain
[9] Miguel Hernandez Univ Elche, CIBERDEM, Alicante, Spain
[10] Univ Parma, Dept Neurosci, Parma, Italy
[11] Univ Turin, Dept Neurosci, Turin, Italy
[12] Univ Turin, Neurosci Inst Cavalieri Ottolenghi, Turin, Italy
[13] Univ Chicago, Dept Med, Sect Endocrinol Diabet & Metab, Chicago, IL 60637 USA
[14] Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Dept Environm Hlth Sci, Amherst, MA 01003 USA
[15] Univ Missouri, Dept Biol Sci, Columbia, MO USA
关键词
Endocrine disruptors; Obesogens; Metabolism disruptors; Developmental origins of health and disease; Obesity; Diabetes; Lipid disorders; PERSISTENT ORGANIC POLLUTANTS; BISPHENOL-A EXPOSURE; BODY-MASS INDEX; PROLIFERATOR-ACTIVATED RECEPTOR; FATTY LIVER-DISEASE; STIMULATED INSULIN-SECRETION; NONMONOTONIC DOSE-RESPONSES; IN-UTERO EXPOSURE; EPIGENETIC TRANSGENERATIONAL INHERITANCE; TOXICANT-ASSOCIATED STEATOHEPATITIS;
D O I
10.1016/j.reprotox.2016.10.001
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The recent epidemics of metabolic diseases, obesity, type 2 diabetes(T2D), liver lipid disorders and metabolic syndrome have largely been attributed to genetic background and changes in diet, exercise and aging. However, there is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of these metabolic diseases. This review will examine changes to the incidence of obesity, T2D and non-alcoholic fatty liver disease (NAFLD), the contribution of genetics to these disorders and describe the role of the endocrine system in these metabolic disorders. It will then specifically focus on the role of endocrine disrupting chemicals (EDCs) in the etiology of obesity, T2D and NAFLD while finally integrating the information on EDCs on multiple metabolic disorders that could lead to metabolic syndrome. We will specifically examine evidence linking EDC exposures during critical periods of development with metabolic diseases that manifest later in life and across generations. Published by Elsevier Inc.
引用
收藏
页码:3 / 33
页数:31
相关论文
共 610 条
[51]   Back to the Future: Moving Beyond "Mesenchymal Stem Cells" [J].
Bianco, Paolo .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2011, 112 (07) :1713-1721
[52]   Developmental Origins of the Adipocyte Lineage: New Insights from Genetics and Genomics Studies [J].
Billon, Nathalie ;
Dani, Christian .
STEM CELL REVIEWS AND REPORTS, 2012, 8 (01) :55-66
[53]   Thyroid and Obesity: An Intriguing Relationship [J].
Biondi, Bernadette .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2010, 95 (08) :3614-3617
[54]   Environmental Chemicals: Evaluating Low-Dose Effects [J].
Birnbaum, Linda S. .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2012, 120 (04) :A143-A144
[55]   Obesogens, stem cells and the maternal programming of obesity [J].
Blumberg, B. .
JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE, 2011, 2 (01) :3-8
[56]   Adult exposure to tributyltin affects hypothalamic neuropeptide Y, Y1 receptor distribution, and circulating leptin in mice [J].
Bo, E. ;
Farinetti, A. ;
Marraudino, M. ;
Sterchele, D. ;
Eva, C. ;
Gotti, S. ;
Panzica, G. .
ANDROLOGY, 2016, 4 (04) :723-734
[57]   Acute exposure to tributyltin induces c-fos activation in the hypothalamic arcuate nucleus of adult male mice [J].
Bo, E. ;
Viglietti-Panzica, C. ;
Panzica, G. C. .
NEUROTOXICOLOGY, 2011, 32 (02) :277-280
[58]   Transmaternal Bisphenol A Exposure Accelerates Diabetes Type 1 Development in NOD Mice [J].
Bodin, Johanna ;
Bolling, Anette Kocbach ;
Becher, Rune ;
Kuper, Frieke ;
Lovik, Martinus ;
Nygaard, Unni Cecilie .
TOXICOLOGICAL SCIENCES, 2014, 137 (02) :311-323
[59]   Long-term bisphenol A exposure accelerates insulitis development in diabetes-prone NOD mice [J].
Bodin, Johanna ;
Bolling, Anette Kocbach ;
Samuelsen, Mari ;
Becher, Rune ;
Lovik, Martinus ;
Nygaard, Unni Cecilie .
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY, 2013, 35 (03) :349-358
[60]   Prenatal air pollution exposure induces sexually dimorphic fetal programming of metabolic and neuroinflammatory outcomes in adult offspring [J].
Bolton, Jessica L. ;
Auten, Richard L. ;
Bilbo, Staci D. .
BRAIN BEHAVIOR AND IMMUNITY, 2014, 37 :30-44