Posted: 2/15/12 | Updated: 2/16/12
The modern lifestyle of super-sized french fries and couch potatoes often takes the blame for the rising rates of obesity and diabetes in the U.S. -- perhaps rightly so. But growing evidence suggests another factor in the dual epidemics: modern chemicals.
Exposure to even minuscule amounts of synthesized substances -- used in everything from pesticides to water bottles -- can scramble hormone signals, scientists say. This interference can trick fat cells into taking in more fat or mislead the pancreas into secreting excess insulin, a hormone that regulates the breakdown of fat and carbohydrates.
Among the most ubiquitous and scrutinized of these so-called endocrine disruptors is bisphenol A, better known as BPA. The chemical is a common ingredient in plastics and food-can linings.
"When you eat something with BPA, it's like telling your organs that you are eating more than you are really eating," says Angel Nadal, a BPA expert at the Miguel Hernandez University in Spain.
Nadal's latest research, published last week in PLoS ONE, finds that the chemical triggers the release of almost double the insulin actually needed to break down food. High insulin levels can desensitize the body to the hormone over time, which in some people may then lead to weight gain and Type 2 diabetes.
Huffington for the rest.
1 Instituto Bioingeniería and CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Universidad Miguel Hernández de Elche, Elche, Alicante, Spain, 2 Institut D'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and CIBERDEM, Barcelona, Spain, 3 Department of Clinical Sciences, Lund University, Malmö, Sweden, 4 Department of Cell Biology and Biochemistry, Center for Nuclear Receptors and Cell Signaling, University of Houston, Houston, Texas, United States of America
Bisphenol-A (BPA) is a widespread endocrine-disrupting chemical (EDC) used as the base compound in the manufacture of polycarbonate plastics. It alters pancreatic β-cell function and can be considered a risk factor for type 2 diabetes in rodents. Here we used ERβ−/− mice to study whether ERβ is involved in the rapid regulation of KATP channel activity, calcium signals and insulin release elicited by environmentally relevant doses of BPA (1 nM). We also investigated these effects of BPA in β-cells and whole islets of Langerhans from humans. 1 nM BPA rapidly decreased KATP channel activity, increased glucose-induced [Ca2+]i signals and insulin release in β-cells from WT mice but not in cells from ERβ−/− mice. The rapid reduction in the KATP channel activity and the insulinotropic effect was seen in human cells and islets. BPA actions were stronger in human islets compared to mouse islets when the same BPA concentration was used. Our findings suggest that BPA behaves as a strong estrogen via nuclear ERβ and indicate that results obtained with BPA in mouse β-cells may be extrapolated to humans. This supports that BPA should be considered as a risk factor for metabolic disorders in humans.
Damn. I do not understand some of that. =)
Glad someone's keeping tabs on what I don't.