New treatment could restore insulation secretion in type 2 diabetics

by Barbara Hewitt on October 17, 2014

A new treatment for type 2 diabetes, which targets the disease mechanism itself and not just the symptoms, is being tested by scientists in Sweden.

For the first time, knowledge about the individual patient’s genetic risk profile is being used by researchers at Lund University. This could mean a treatment that completely restores the capacity to secrete insulin in those who have an impaired risk gene.


The treatment may restore the capacity to secrete insulin in those who have an impaired risk gene

‘The concept of treatment personalised to the individual’s risk profile has great potential. Our results show that it is possible to block the effects of a common risk gene for type 2 diabetes,’ said Anders Rosengren, the diabetes researcher at Lund University in charge of the project.

A milestone was an article in the journal Science in 2009. At the time, several research teams from Lund University were able to report that a common gene variant in the population makes insulin-producing cells sensitive to stress hormones. This greatly impairs the cells’ capacity to secrete insulin.

Continued work showed that Yohimbin, a drug that had been deregistered for several years, effectively blocked the gene variant’s damaging effects both in animal experiments and in experiments with donated human insulin-producing cells. When Yohimbin was administered, the capacity to secrete insulin improved.

The gene variant is common, with around 30% of the population having it, and it’s even more frequent in patients with type 2 diabetes. Out of 400, 000 people in Sweden who have type 2 diabetes, some 40% of patients are carriers.

‘The fact that this was an old drug made this journey a lot faster. The substance had already been tested for safety and approved,’ said researcher Erik Renström, adding that with a known disease mechanism and a method to neutralise it, the obvious next step was to test it on patients.

Some 50 patients with type 2 diabetes were recruited for the study, of which 21 did not have the risk variant, while the remainder were carriers. All of them underwent a glucose tolerance test, which shows how well insulin secretion responds to excess sugar load. Not unexpectedly, the secretion was 25% worse in patients who had the risk gene.

Subsequently, all participants in the study were given either Yohimbin or a placebo on three different occasions and insulin secretion was registered again.

‘Yohimbin neutralised the effects of the risk gene. The carriers of the risk gene gained the same capacity to secrete insulin as those without the risk variant,’ said Yunzhao Tang, principal author of the study.

‘Yohimbin must be modified to minimise side effects, in this case raised blood pressure, and we need the help of a cooperation partner to achieve this. The substance must also be tested on more patients before it can become a clinical drug,’ Rosengren explained.

‘Purely theoretically, the drug should be effective for the 40% of type 2 diabetes sufferers who are carriers of the genetic risk variant,’ he added.

The opinions expressed in this article do not necessarily reflect the views of the Community and should not be interpreted as medical advice. Please see your doctor before making any changes to your diabetes management plan.

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