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Biological Chemistry

Study Firms Up BPA-Diabetes Link

Tests on mouse and human cells find that the estrogen mimic stimulates an increase in insulin production

by Stephen K. Ritter
February 13, 2012 | APPEARED IN VOLUME 90, ISSUE 7

A lab study designed to examine the relationship between bisphenol A (BPA) and insulin regulation leading to diabetes has found that the controversial chemical increases insulin release, more so in human cells than in mouse cells (PLoS One, DOI: 10.1371/journal.pone.0031109). BPA is a synthetic chemical building block used to make an array of consumer products, especially polycarbonate plastics for food packaging. It has been found at low levels in the blood and urine of most people and is linked to several diseases. Scientists have struggled to understand how BPA affects physiological processes and to determine with certainty whether BPA should be considered a health hazard. Angel Nadal of Spain’s Miguel Hernández University of Elche and coworkers found that nanomolar amounts of BPA, on the order of that found in people, interferes with estrogen receptors to decrease the activity of potassium ion channels, increase glucose-induced calcium signaling, and trigger increased insulin release from pancreatic β-cells—conditions that lead to diabetes. Nadal’s team says its findings show that BPA acts as a strong estrogen similar to the natural hormone estradiol and support the idea that BPA should be considered a risk factor for metabolic disorders in humans.

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