Published August 25, 2014
University at Buffalo researchers are studying how chemicals in the environment may raise the risk of prevalent metabolic conditions by disrupting neuroendocrine circadian functions and altering the release of hormones, including insulin.
“Our results may help clarify some of the causes behind the epidemic we are experiencing in Type 2 diabetes, obesity and metabolic syndrome,” says Margarita L. Dubocovich, PhD, SUNY Distinguished Professor and chair of pharmacology and toxicology.
She and Rajendram V. Rajnarayanan, PhD, assistant professor of pharmacology and toxicology, were awarded a two-year, $436,751 grant from the National Institute of Environmental Health Sciences to conduct the study.
Dubocovich describes the study as a “hunt for environmental chemicals that affect melatonin’s actions.” Melatonin is a circadian hormone that functions as a sleep and circadian rhythms regulator.
“The goal is to identify environmental chemicals that alter the ability of the nocturnally-produced melatonin to transmit signals of darkness to target tissues, such as pancreatic beta cells,” she says.
The results could lead to regulatory guidelines for chemicals that disrupt this ability.
“Many of these chemicals are flying under the toxicological radar and have no established guidelines for exposure,” says Rajnarayanan.
The research will bring together big data on millions of chemicals to find which ones are circadian disruptors and may be causing diabetes, explains Rajnarayanan.
“We are merging our expertise to establish a comprehensive pharmacoinformatics pipeline — which we call Chem2Risk — to leverage big data on toxic chemical exposure,” he says.
The multidisciplinary UB team has expertise in the neurobiology of melatonin as well as integrated computational modeling of chemicals that bind to melatonin receptors.
Dubocovich has specialized in studying melatonin and its receptors in the brain and peripheral organs. She has pioneered the discovery of drugs to study the functional role of melatonin receptors.