Potential mechanisms that contribute to 'I am full' feeling identified
Washington, Mar 4 (ANI): Researchers from the University of Pennsylvania are one step closer to developing effective, FDA-approved treatments for obesity.
They have identified the neurological and cellular signalling 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.
The researchers believe more comprehensive knowledge of these mechanisms could form the basis for future anti-obesity medications.
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 behaviour.
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," said lead author Matthew Hayes.
"Ignoring the brain is not the right strategy, as these drugs are certainly engaging multiple, distributed centers in the brain governing energy balance regulation," said co-author Harvey Grill.
The Penn group not only identified a necessary part of the brain which mediates the food intake suppression effect produced by these drugs, the nucleus tractus solitarius, or NTS, but also the cellular signalling pathways required for production of GLP-1's satiety effects.
That the Penn researchers were able to demonstrate a potential neurochemical mechanism of weight loss for a class of drugs already used in the treatment of type 2 diabetes provides a missing piece of the puzzle for future FDA-approved anti-obesity drugs.
"If we can identify other chemical signals or hormones that act on the same pathways that we've shown here, then by combined action you have a coordinated, orchestrated symphony of weight suppression," said Hayes.
The study is published in the March 2 edition of the journal Cell Metabolism. (ANI)
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