Flame retardant chemicals used in electronics could be contributing to the growing public health problem of overweight and obesity. That’s according to University of Houston researchers who have discovered that a common flame retardant used in circuit boards for electronic devices may be partly to blame for ballooning BMIs in the information age. Scientists at UH’s Center for Nuclear Receptors and Cell Signaling (CNRCS) have been investigating the issue by studying zebrafish.
Overweight zebrafish? — you might be asking. Zebrafish are an emerging rock star of biological and genetic research — a species with many lab-friendly qualities such as hardiness, being native to India’s sewage-infested Ganges River in India, and also known as a beginner’s fish, because they’re cheap, don’t die easily, weather extreme heat and tolerate low-oxygen tension. Zebrafish also produce transparent embryos, enabling researchers using microscopes to directly observe the effects of altering specific gene functions and to sidestep the messy process of studying mice embryos: scooping them out of the dead mother.
The zebrafish model system offers advantages for conducting forward and reverse genetics, gene misexpression, transgenics, and numerous cell biological approaches, and while the zebrafish model system is relatively new, hundreds of zebrafish labs are reportedly operating worldwide. For more information, visit the zebrafish model organism database, the Zebrafish Information Network (ZFIN) and this article.
The UH researchers, supported by a $375,209 grant from the National Institutes of Health’s National Institute for Environmental Health Sciences (NIEHS), looked for compounds that lead to obesity, called obesogens, studying the effect that two common flame retardants produced in sibling zebrafish. The fish they exposed to the chemicals became heavier and longer, compared to their untreated siblings used as a control group.
A variant of the compound bisphenol A (BPA), which has already been flagged as an obesogen, are produced and introduced to the environment in massive quantities, with 150,000 tons of TBBPA and 10,000 tons of TCBPA being produced annually according to the UH researchers.
“It’s been shown that young children, who spend a lot of time on the floor, have higher levels of these compounds in their blood than adults. It has also been found to be passed through breast milk,” explains Dr. Maria Bondesson, a research assistant professor of biology and biochemistry at the CNRCS in a UH release. “This is what led us to exposing the fish siblings to these compounds at relatively low concentrations. The fish treated with these compounds became heavier and the ones that weren’t were lighter.”
Dr. Bondesson notes that consumers are constantly exposed to thousands of industrial chemicals, with a major exposure route being through different foods we eat. Many of these chemicals interact with the human body’s fine-tuned hormone system and are consequently referred to as “endocrine disrupting chemicals.”
She cites previous research indicating that these endocrine disrupting chemicals contribute to a wide array of human diseases, including but not limited to obesity, atherosclerosis, type 2 diabetes, osteoporosis, breast-, prostate-, and colon cancer, and reproductive disturbances.
“These diseases are becoming increasingly common and are a considerable burden on society and the economy at a global level, Dr. Bondesson observes. “My research interest is to study how environmental pollutants affect human health. We are currently running several research projects on environmental pollutants. In the first project we study how the endocrine disrupting chemical bisphenol A in combination with phytoestrogens affect signaling of the estrogen receptors. The second project uses zebrafish as a model system to detect chemical pollutants that perturb embryonic development (or more information on this project see http//tivs-center.uh.edu/). In a third project we develop zebrafish screening methods for detection of chemicals that cause obesity and diabetes.”
In the NIEHS-funded study, the UH researchers treated zebrafish with the suspected flame-retardant obesogens for eleven days, feeding them a diet of egg yolks as a fat source — then stained the fish for lipids, or fat cells. They report that despite both fish being fed a high-cholesterol diet, the normal fish didn’t accumulate lipids in their bodies the way the flame retardant treated fish did. This observation led the research team to determine that it was indeed the chemical obesogens and not the die itself that caused the chemical-exposed fish to gain weight.
“The transparency of the zebrafish allowed us to see where the increased amounts of fat cells were. There was an enormous difference between the treated fish and their siblings in the control group,” says Dr. Bondesson. “We could see the lipids accumulated in the liver, the heart region, the head and very obviously in the blood vessels. We also could see it subcutaneously along the side of the fish. ”
After an initial 11 days of exposure to the flame retardants, the scientists stopped exposing the fish to the suspected obesogens, Within a month of being kept under equal and normal conditions, the fish that had been previously exposed to the flame retardants were still heavier and longer than their siblings, and more heavy than long, so their BMI was higher as well.
The scientists maintain that the mechanism at the root of these observed phenomena is a hormone receptor called “PPARgamma,” which has a capacity to turn stem cells into adipocytes, more commonly known as fat cells. Previous studies have demonstrated that flame retardants like TBBPA and TCBPA can activate this hormone receptor. Dr. Bondesson, together with Department of Biosciences & Nutrition professor Jan-Ake Gustafsson and their team, hypothesizes that these flame retardants serve as a biochemical trigger that signals for fat cells to form and thereby function as obesogens. Her UH group is the first to test this theory in a living organism.
“Given the growing obesity epidemic and the serious health conditions it often leads to, our research shows that its important to study if chemicals are obesogens,” Dr. Bondesson says, “our goal is to find the worst ones and then replace them with safer alternatives.”
Working with Drs. Bondesson and Gustafsson on this study were fellow CNRCS researchers Catherine McCollum, Anne Riu and Caroline Pinto, in collaboration with researchers from France.
Dr. Bondesson also recently attended an NIEHS-hosted Institute of Medicine workshop on environmental exposures leading to obesity held March 2-3 in North Carolina, and where scientific presentations explored the role of chemical exposures in obesity development.
The University of Houston
The University of Houston