Scientists believed that diseases such as obesity and fatty liver disease were the result of anomalies in the metabolism of lipids that was triggered by excessive energy intake, fat consumption and a lack of physical activity; this study reveals the existence of chemical compounds that humans are exposed to in a variety of consumer products that can lead to lipid related metabolic diseases and weight gain.
“Previous studies have provided strong evidence linking some hormone-like compounds to obesity in humans, but this is the first study that showed a cellular and metabolic effect on human cells exposed directly to those compounds,” said Ramon Lavado, Ph.D., assistant professor of environmental science at Baylor.
The researchers have been conducting studies to investigate whether obesogens prompt dysregulation of lipids in the human liver. Poor nutrition and lack of exercise are known contributors to obesity, now emerging evidence is suggesting potential effects of some chemical compounds triggering lipid related diseases. Exposure to obesogens were found to disrupt normal metabolic processes and to increase susceptibility to weight gain across lifespan, says Lavado.
According to research published in Environmental Science & Technology as of 2000 globally there were an estimated 100,000 commercially available chemicals, this amount has more than tripled since then with some 350,000 chemicals now being available.
Disease contributing chemicals can be found in cigarette smoke, air pollution, pesticides, fungicides, flame retardants and certain classes of chemicals used in many consumer products to make them softer; other contributors widely used are in industrial chemicals found within paints, cements, fluorescent light ballast, sealants, and adhesives.
Well established techniques in the field of metabolomics and molecular toxicology were used to investigate whether the proportion of lipids related to diseases were modified upon exposure to environmental obesogens, and to what extent the lipid profile was changed if it was modified. Fluorescence microscopy was also used to investigate whether environmentally relevant concentrations of tested compounds had the ability to induce fat accumulation in liver tissues.
Findings suggest that production of diglycerides and triglycerides increased significantly while other less harmful lipids were found in smaller proportions; these effects were also observed in cells exposed to chemical concentrations that are often seen in the environment to which humans are constantly exposed to. According to Lavado this study is among the first to report molecular and physical changes at a cellular level as well as the quantification of specific types of lipids that emerge as a result of chemical exposure.
“In the case of lipid profile alterations, the idea that chemical compounds may trigger and/or contribute to the development of lipid-related diseases deserves extensive research in the future,” he said. Adding that the study supports further study using animal alternatives with more relevance to humans as a tool to characterize the health effects caused by these chemicals that humans are often exposed to but lack a thorough toxicological data.
