- A common diabetes drug has been found to curb cocaine use, study says
- The drug Byetta is derived from a natural hormone called GLP-1
- That hormone regulates feeding behavior, according to scientists
- They gave cocaine-addicted rats Byetta – and found reduced cocaine use
- This finding suggests cocaine intake can also be regulated by GLP-1
Lisa Ryan For Dailymail.com
18:02 EST, 11 February 2016
22:39 EST, 11 February 2016
Cocaine addiction and diabetes are not frequently associated.
Yet, a common drug used to treat diabetes has been found to also help reduce cocaine dependence.
Scientists have revealed that Byetta, a drug currently used on obese patients and type 2 diabetics, is derived from a naturally occurring hormone called glucagon-like peptide-1, or GLP-1.
GLP-1 regulates feeding behaviors – and University of Pennsylvania scientists discovered it also plays a rule in cocaine consumption.
Scientists found that rats who had been fed cocaine had a decrease in their cocaine self-administration after taking Byetta.
Because the drug is already safe for human use, this could lead to new addiction treatments.
Byetta is a drug used to treat type 2 diabetes and obesity by targeting GLP-1, a hormone that regulates food consumption. Scientists gave the drug to rats hooked on cocaine – and found they lowered their self-administered cocaine intake
A previous study used GLP-1 to compare a person’s consumption of a burger and fries – palatable food – to a salad.
The scientists determined that activating GLP-1 receptors in a specific part of the brain reduced a person’s intake of burger and fries.
However, activating GLP-1 had no effect on salad consumption.
Furthermore, past research suggested there is an overlap between neural circuits that influence feeding and drug taking.
Thus, the scientists formed a straightforward hypothesis.
Study co-author Dr Heath Schmidt said: ‘If GLP-1 regulates intake of palatable food, then perhaps it also regulates consumption of cocaine. That was it in a nutshell.’
The study was conducted over the course of two-and-a-half years.
The scientists found that when they activated GLP-1 receptors in the ventral tegmental area – or VTA, the area of the brain that deals with reward behavior – rats wanted less cocaine.
This study was the first time that GLP-1 has been shown to effect drug consumption in the brain.
GLP-1 reacts similarly in rat and human brains, according to the study.
And so, rather than injecting cocaine, the scientists offered the rats a lever to press for intravenous infusions.
It was after the animals were stabilized in their drug-taking regimen that the GLP-1 receptor agonist was introduced into their brains.
Dr Schmidt said: ‘We’re looking at what activating of GLP-1 receptors in the VTA does to the animal’s self-administration of cocaine.
‘We were able to show a nice decrease in cocaine self-administration.’
Previous research suggested that there was an overlap in brain circuitry that regulates food and drug consumption. The study may lead to new treatments for cocaine addiction
No human trials have been completed yet; however, the scientists noted that the drug’s US Food and Drug Administration approval may make human trials more likely.
Dr Schmidt said: ‘Our interest is really to understand how chronic exposure to drugs of abuse changes the brain to produce addiction-like behaviors.’
The team of scientists is hoping to next focus on their research on the pathway GLP-1 follows in the brain.
Dr Schmidt said: ‘That gets into a systems neuroscience approach, into the circuitry underlying the behavior.
‘It’s really provocative… We talk about the VTA and the reward circuit that drives cocaine taking.
‘But there’s also this pathway that cocaine is activating that’s functioning as a “brake” to try and stop or reduce the behavior.’
The study was published in the journal Neuropsychopharmacology.