Table 2.
Synthesis of various endocrine-disrupting chemicals (EDCs) and some of their characteristics and adverse metabolic effects in relation with the adipose tissue as presented Section 3, Section 4, Section 5 and Section 6.
| Chemicals | Examples | Degradability and Route of Exposure | Sources | Possible Mechanisms Relevant for Energy Metabolism | In Vitro Effects Potentially Described (Mostly Using 3T3-L1 Cells) | In Vivo Metabolic Effects Potentially Described on Body Weight/Fat Mass | Ref. |
|---|---|---|---|---|---|---|---|
| Dioxins and dioxin-like PCBs | 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); coplanar PCB-77, 126 | Persistent; exposure through diet (mainly) | Dioxins: industrial by-products, forest fires, volcanic eruption; DL-PCBs: industrial products in electrical capacitors | AhR; cross-interaction with PPARγ and ERs | Alteration of adipogenesis; adipocyte cell size; levels of inflammatory markers and resistance to insulin | Obesogen at low doses (≠high and acute exposure); changes in body weight and/or body fat composition in both sexes depending on period of exposure (maternal or post-weaning); effects on microbiota | [91,92,93,94,95,96,97,98,99,100,101,159,205,207,211,214] |
| Non-dioxin like PCBs | PCB153; PCB101; PCB180 | Persistent; exposure mainly from diet | Industrial products used for their low-flammability and high conductivity properties | Estrogen and thyroid signaling; indirect effect via PXR and CAR; RXR and retinoid signaling | changes in adipocyte cell size; inflammatory markers, lipid metabolism; | Obesogen in males; Increased adipocyte differentiation; alteration of retinoid synthesis and of lipid metabolism | [11,70,95,102,104,105,158] |
| Organochlorine pesticides | DDT and its metabolite DDE | persistent; bioaccumulation through the food chain | agricultural pesticides | Sex steroid and thyroid hormone pathways; PPAR | Alteration of adipogenesis; enhancement of adipogenesis and induction of unhealthy mature adipocytes | Impaired metabolic homeostasis in female but not in male mice after perinatal exposure to DDT | [109,146,147,181] |
| Organotin compound | Tributiltyn (TBT); dibutyltin (DBT) | Persistent | Powerful biocide; marine shipping applications as fungicides; diet exposure | PPARs, RXRs, ERs | Alteration of adipocyte lineage commitment in a RXR-dependent manner; promotion of adipogenesis in a PPARγ-dependent manner but not all of the health-promoting activities induced by Pparγ resulting in unhealthy adipocytes; | Obesogen in both sexes; adipocyte lineage commitment; adipocyte differentiation; epigenetic mechanisms and transgenerational effects; effects on microbiota | [110,111,112,113,114,115,209,210] |
| Flame retardants | Polybrominated flame retardants (PBDEs; TBBPA; EHDPHP) | Persistent | Added to manufactured materials such as plastics, textiles to delay development of ignition; present in house dusts; | Estrogen and thyroid hormone pathways; PPARγ, GR, PXR | Lipid accumulation; enhanced adipogenesis and expression of markers of adipogenesis; enhances oxidative stress | Enhanced body weight; reduced glucose uptake; enhances the expression of inflammatory markers; triglyceride synthesis; bile secretion; effects on microbiota | [11,70,106,107,108,141,142,143,148,212,215] |
| Phenylsulfamides | Tolylfluanid (TF) | Not persistent | Active ingredient in fungicides and wood preservatives | GR; mitochondrial metabolism | Obesogen in vivo; | Increased adipocyte differentiation; sex-dimorphism | [130,192,193,194] |
| Phthalates | DEHP | Short half-life; exposure through diet and hand-to-mouth behavior in children | Plastic components, cosmetics, medical equipment | PPARs, CAR/PX, GR | exposure is associated with metabolic-related disturbances | Adipocyte differentiation; sex-dimorphism; effects on microbiota | [123,125,127,128,129,130,208,213] |
| Bisphenols | BPA, BPS | Short half-life; exposure through diet and water drinking because of leaching of the chemical from cans, plastic bottle. | Plastic components, cosmetics, disinfectants, thermal paper receipts | ERs and estrogen related receptors (ERRs), AR, TR, GR, PPARγ | BPA can increase metabolic disturbances within insulin-sensitive organs including the adipose tissue eventually leading to type 2 diabetes without systematically causing gain of weight; evidences for obesogenic properties of BPS | Adipocyte differentiation; Insulin sensitivity; expression of adipogenic and inflammatory markers; ex-dimorphism; effects on microbiota | [117,118,119,120,121,122,123,124,125,126,130,131,132,133,134,135,136,137,183,184,185,186,187,206,212] |