PHILADELPHIA An interdisciplinary group of researchers at the University of Pennsylvania has, for the first time, identified the neurological and cellular signaling mechanisms that contribute to satiety the sensation of feeling full and the subsequent body-weight loss produced by drugs used to treat type 2 diabetes. More comprehensive knowledge of these mechanisms could form the basis for anti-obesity medications.
The group was led by Matthew Hayes of the School of Medicine's Psychiatry Department, Harvey Grill of the Psychology Department in the School of Arts and Sciences and Kendra Bence of the School of Veterinary Medicine's Animal Biology Department. Their research was aided by a team of postdoctoral and doctoral fellows, as well as technicians and undergraduate students at Penn.
The study was published in the March 2 edition of the journal Cell Metabolism.
While no pharmaceutical treatment for obesity currently exists, type 2 diabetes drugs targeting the hormone glucagon-like-peptide-1, or GLP-1, for insulin production may hold promise. These drugs were known to promote weight loss, simply as a result of patients eating less. Researchers, however, could not explain exactly what caused this change in behavior.
Naturally occurring GLP-1 is made in primarily two distinct locations in the body, the gut and the brain. Much of the previous research in this area has focused on the former at the expense of the latter when attempting to identify the relevant population of GLP-1 receptors that may mediate the suppression in food intake by pharmaceutical GLP-1 drugs.
"Identifying both the site-of-action and mechanisms that accounts for the body weight loss of these GLP-1 drugs puts us one step closer to developing effective, FDA-approved, treatments for obesity," Hayes said.
"Ignoring the brain is not the right strategy, as these drugs are certainly engaging multiple, distributed centers in the bra
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University of Pennsylvania