Thursday December 13, 2018

Alcohol addiction could be treated with diabetes medication

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By NewsGram Staff Writer

London: A new research suggested that the medication for diabetes and obesity can treat alcohol dependency.

Swedish researchers identified that interfering with the hormone GLP-1 could be a target for treating alcohol dependence.Researchers have found that a medication that resemble GLP-1, which is used to treat Type-2 diabetes as well as obesity, also could be used to treat alcohol dependence.

fb72ediabetes-photoAlcohol dependence causes morbidity as well as mortality and is a major health problem in today’s society.

“We suggest that medications that resemble GLP-1 could be used to treat alcohol dependence in humans,” said one of the researchers Elisabet Jerlhag from Sahlgrenska Academy, University of Gothenburg in Sweden.

Usually, dopamine is released in the brain’s reward center in response to drinking alcohol, which leads to a sense of euphoria.

The GLP-1-like substance prevents the ability of alcohol to increase dopamine in reward areas in the mice, suggesting that they no longer experience a reward from alcohol, the findings showed.

“The GLP-1-like substance reduced the alcohol consumption by 30-40 percent in rats that drank large quantities of alcohol for several months,” Jerlhag noted.

The researchers found that the diabetes medication also reduced the motivation to drink alcohol in rats that were bred to drink a lot of alcohol. The medication also prevented relapse drinking in rats, which is major problem for alcohol dependent individuals.

The study was published in the journal Addict Biology.

(With inputs from IANS)

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New Drug Offers Treatment For Diabetes-Related Blindness

The researchers now plan to conduct a full-scale clinical trial, Gamble said

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New drug offers hope for diabetes-related blindness.

In a major breakthrough, Australian scientists have developed a new drug that offers treatment for people suffering from diabetic retinopathy — the main cause of blindness from diabetes.

The debilitating disease occurs when tiny blood vessels in the retina, responsible for detecting light, leak fluid or haemorrhage.

While treatment options include laser surgery or eye injections of anti-vascular endothelial growth factor (VEGF), they are not always effective or can result in side effects, highlighting the need for alternative therapeutic approaches.

The team from the Centenary Institute in Sydney developed a novel drug CD5-2, which in mouse models was found to mend the damaged blood retinal barrier and reduce vascular leakage.

“We believe CD5-2 could potentially be used as a stand-alone therapy to treat those patients who fail to respond to the anti-VEGF treatment. It may also work in conjunction with existing anti-VEGF treatments to extend the effectiveness of the treatment,” said lead author Ka Ka Ting from the Institute.

“With limited treatment options currently available, it is critical we develop alternative strategies for the treatment of this outcome of diabetes,” Ting added.

Diabetes
Representational image. Pixabay

The key process involved in diabetic retinopathy pathology is the breakdown of the blood-retinal barrier (BRB), which is normally impermeable. Its integrity relies on how well capillary endothelial cells are bound together by tight junctions. If the junctions are loose or damaged, the blood vessels can leak.

In the study, reported in the journal Diabetologia, CD5-2 was found to have therapeutic potential for individuals with vascular-leak-associated retinal diseases based on its ease of delivery and its ability to reverse vascular dysfunction as well as inflammatory aspects in animal models of retinopathy.

Previous studies have shown that CD5-2 can have positive effects on the growth of blood vessels.

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“This drug has shown great promise for the treatment of several major health problems, in the eye and in the brain,” said Professor Jenny Gamble, head of Centenary’s Vascular Biology Programme.

The researchers now plan to conduct a full-scale clinical trial, Gamble said. (IANS)