Exposure BPA BADGE causes obesity
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Exposure to BPA and BADGE causes obesity

5:15 AM, 30th May 2012
Exposure to BPA and BADGE causes obesity
Exposure to BPA and BADGE causes obesity.

NORTH CAROLINA, US: Bisphenol A (BPA) and bisphenol A diglycidyl ether (BADGE) are used for the manufacturing of coating and resins and leach from packaging materials into food. Numerous studies have suggested that BPA and BADGE may have adverse consequences on human health, including the possibility that exposure to such chemicals could be superimposed on traditional risk factors to initiate the development of obesity.

BPA, a potentially toxic estrogen-mimicking compound used in plastic production, has been linked to obesity in the past. BPA is in everything from soup cans to store receipts. But the worst thing is, a chemical that breaks down into BPA can cause stem cells to become fat cells. And we’re exposed to a whole lot more of that chemical than BPA.

The researchers sought to test the adipogenic effects of BADGE in a biologically-relevant cell culture model. For this, they used multipotent mesenchymal stromal stem cells (MSCs) to study the adipogenic capacity of BADGE and BPA and evaluated their effects on adipogenesis, osteogenesis, gene expression and nuclear receptor activation. We are exposed to enough BADGE in our daily lives that it could make a difference in the obesity epidemic. Exposure to these kinds of chemicals (obesogens) can reprogramme the metabolism and make it more likely to store calories instead of passing them through.

BADGE is far from the only known obesogen. Others include BPA, sugar, nicotine, certain pesticides, perfluorooctinoates (found in non-stick cookware and greaseproof coatings, among other places), MSG, and estrogens like DES and genistein (found in soybeans, fava beans, and coffee).

BADGE induced adipogenesis in mouse and human MSCs, as well as in mouse 3T3-L1 preadipocytes. In contrast, BPA failed to promote adipogenesis in MSCs, but induced adipogenesis in 3T3-L1 cells. BADGE exposure elicited an adipogenic gene expression profile and its ability to induce adipogenesis and expression of adipogenic genes was not blocked by known PPARγ antagonists. Neither BADGE nor BPA activated or antagonized RXR or PPARγ in transient transfection assays.

They concluded that BADGE can induce adipogenic differentiation in both MSCs and in preadipocytes at low concentrations, comparable to those that have been observed in limited human biomonitoring. BADGE probably acts through a mechanism that is downstream of, or parallel to PPARγ. Put it all together, it is pretty convincing that toxic chemicals are making us fat. It could be some combination of chemical exposure and following incorrect dietary recommendations.

© Environmental Health Perspectives News

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