Copyright
©The Author(s) 2017.
World J Biol Chem. May 26, 2017; 8(2): 108-119
Published online May 26, 2017. doi: 10.4331/wjbc.v8.i2.108
Published online May 26, 2017. doi: 10.4331/wjbc.v8.i2.108
Chemicals | Sources | Examples | Some demonstrated metabolic effects |
Alkylphenols | Lubricating oil additives; detergents; emulsifiers, pesticides; plastics Exposure occurs via water drinking and food consumption[67] | NP | Estrogenic activities[68] |
Dioxins | Byproducts of industries from incomplete combustion; release during natural events such as wood burning and volcanic eruption Diet is the main route of exposure[69] | TCDD | Hepatic steatosis[70] and fibrosis[71]; increased adipocyte differentiation (in vitro)[72] |
Flame retardants | Used in electronic equipment, furniture, plastics…and then, present in dust, air and soil Dermal exposure is a significant route of exposure[73] | Penta-BDE | Decrease in glucose oxidation[74] |
Organotin compound | Used as biocide in anti-fouling paint, heat stabilizer in Poly Vinyl Chloride Exposure mainly by consumption of seafood[75] | TBT | Induction of adipocyte differentiation[76]; increase of body weight and hepatic steatosis[77]; transgenerational effects on fat depots and hepatic steatosis[39] |
Phenolic derivatives | Plastic components, cosmetics, disinfectants, thermal paper receipts Food and water drinking are the major routes of exposure[78] | BPA, BPS | Estrogenic activities[79]; alteration of pancreatic β cell functions and hepatic insulin signaling (BPA)[47]; induction of lipid accumulation and differentiation (in vitro, BPS)[80] |
Pesticides | Due to their persistence, accumulation in soils and sediments; bioaccumulation throughout the food chain | DDT and its metabolite | Alteration of systemic glucose homeostasis and hepatic lipid metabolism[83]; Glucose intolerance, hyperinsulinemia, dyslipidemia and altered bile acid metabolism[84] |
Processing of agriculture products (banned in Europe); Dietary sources[81] as well as inhalation and dermal routes of exposure[82] | Atrazine (C8H14ClN5) | Increased body weight, intra-abdominal fat and insulin resistance[85] | |
Phthalates | Plastic components, cosmetics, medical equipment; Exposure mainly derives from dietary sources for high molecular weight phthalates (e.g., DEHP) and non-dietary sources for low molecular weight phthalates (e.g., DBP)[86] | DBP, DEHP | Anti-androgenic effects[87]; Transgenerational inheritance of obesity[88]; Increased adipocyte differentiation[89] |
PCBs | Synthetic compounds now banned but previously used, in particular, in electrical capacitors; still release in environment due to their persistence Food consumption contributes over 90% of total exposure[90] | PCB153 (C12H4Cl6), PCB170 (C12H3Cl7), PCB187 (C12H3Cl7) (non dioxin-like); PCB126 (C12H5Cl5), PCB77 (C12H6Cl4) (dioxin-like) | Increased adipocyte differentiation (in vitro); increased body weight, adipocyte hypertrophy[72]; increased hepatic steatosis and visceral adiposity in the context of a lipid-enriched diet[91] |
PAH | Byproducts of incomplete combustion of organic compounds (cigarette smoke, wood burning, overcooked meat…) Contamination primarily through inhalation and consumption of certain foods[92] | B[a]P | Carcinogenic Alteration of estrogen metabolism in human mammary carcinoma-derived cell lines[93] Inhibition of lipolysis, increased fat accumulation and weight gain[94] |
PFAA | Water and oil repellent; used for treatments of clothing, insulation and fire-fighting foams Oral and dermal exposure[95] | PFOA | Elevated serum leptin and insulin; overweight after in utero exposure[96] |
Insulin status | Obesity | No body weight change |
Insulin resistance | ERα (-/-) in both males and females[38] | |
No difference in insulin sensitivity | AR (-/-) in males only[97] | |
Improved insulin sensitivity | ERβ (-/-) (study on males only)[26] | CAR activation (study on males only in HFD context, activation by TOBOBOP)[99] |
ERRβ (deletion in neurons; study on males only)[98] | AhR (-/-) (studies on males only)[100] | |
AhR (-/-) (studies on males only, in HFD context)[101] | ||
PPARα (-/-) (studies on males only, in HFD context)[102] | ||
PXR (-/-) (studies on males only, in HFD context)[103] |
Nuclear receptors | Interactions with chemicals |
Steroid receptors | |
ER | BPA (Erα[38], GPR30[104]) |
AR | BPA[105] |
GR | BPA; phthalates[106] |
PR | BPA[107] |
TR | BPA[108]; brominated flame retardants, BFR[109] |
RXR heterodimers | |
PPARα | Phthalates[110]; polyfluoroalkyl compounds[111]; pyrethrins[112] |
PPARγ | Phthalates[110,113]; organotins[76]; BPA[114] |
FXR | Pyrethroids[115] |
CAR | Phthalates[116,117] |
LXRα | Phthalates; BPA[118] |
PXR | Phthalates; BPA[119,120] |
Other receptors | |
AhR | Dioxines; PCB dioxin-like[72,121,122] |
- Citation: Le Magueresse-Battistoni B, Labaronne E, Vidal H, Naville D. Endocrine disrupting chemicals in mixture and obesity, diabetes and related metabolic disorders. World J Biol Chem 2017; 8(2): 108-119
- URL: https://www.wjgnet.com/1949-8454/full/v8/i2/108.htm
- DOI: https://dx.doi.org/10.4331/wjbc.v8.i2.108