Environmental chemicals that may boost diabetes risk by disrupting circadian rhythms are being studied at UB

BUFFALO, N.Y. – Health officials describe diabetes and metabolic disorders as having reached epidemic proportions, often citing diet and lifestyle as culprits.

But environmental chemicals, known as circadian disruptors, may also play a role in soaring rates of obesity, metabolic disorders and Type 2 diabetes.

Now, a University at Buffalo team of researchers has been awarded a federal grant to explore how environmental chemicals that disrupt neuroendocrine circadian functions and hormone release may raise the risk of diabetes and other disorders.

The UB team has expertise in the neurobiology of the circadian hormone melatonin and integrated computational modeling of chemicals that bind to melatonin receptors.

 “Results from this research may help clarify some of the causes behind the epidemic we are experiencing in diabetes and metabolic disorders,” says Margarita L. Dubocovich, PhD, SUNY Distinguished Professor and chair of the Department of Pharmacology and Toxicology in the UB School of Medicine and Biomedical Sciences.

Dubocovich and Rajendram V. Rajnarayanan, PhD, assistant professor of pharmacology and toxicology at UB, are principal investigators on the two-year, $436,751 grant from the National Institute of Environmental Health Sciences, part of the National Institutes of Health.

“Many of these chemicals are flying under the toxicological radar and have no established guidelines for exposure,” says Rajnarayanan.

He explains that the purpose of this grant is to bring together big data on millions of chemicals to find out which ones are circadian disruptors and may be causing diabetes.

“This grant will merge our expertise in order to establish a comprehensive pharmacoinformatics pipeline, which we call Chem2Risk, to leverage big data on toxic chemical exposure,” he continues.

Dubocovich has spent much of her research career studying melatonin, a sleep regulator, and its receptors, and she pioneered the discovery of drugs to assess the functional role of melatonin receptors.

“The goal of this research is to identify environmental chemicals that mimic or affect melatonin and its ability to transmit ‘time-of-day’ messages to target peripheral tissues, such as pancreatic beta cells,” she says.

Dubocovich notes that work on this grant exemplifies the multidisciplinary team approach that UB promotes.

“Science flourishes in an intellectually diverse and collaborative environment,” notes Dubocovich. “Our meetings catalyzed discussions toward the central research question and our hunt for environmental chemicals that mimic melatonin began.”