Obesity Drug Achieves Weight Loss of 24 kg

People with obesity lost 24 kilograms on average when they were treated with the highest dose of a new hunger-blocking drug in a large clinical trial. “It’s really exciting. The weight loss they’re showing is dramatic – it’s as much as you get with successful bariatric surgery,” says Michael Cowley at Monash University in Melbourne, Australia, who wasn’t involved in the research.

The drug used, called tirzepatide, combines synthetic mimics of two hormones known as GLP-1 and GIP that our guts naturally release after we eat to make us feel full. In a late-stage clinical trial, more than 2500 people in nine countries, who weighed 105 kilograms on average at baseline, were asked to give themselves weekly injections of tirzepatide at low, medium or high doses or a placebo for 72 weeks, without knowing which one they were taking.

The highest dose of tirzepatide was most effective, resulting in 24 kilograms of weight loss on average, equivalent to a 22.5 per cent reduction in body weight. In comparison, participants taking the placebo lost just 2 kilograms on average. The results were announced on 28 April by US pharmaceutical giant Lilly, which is developing the drug.

In June 2021, the US Food and Drug Administration approved another obesity drug called semaglutide, which contains a GLP-1 mimic on its own, without the addition of GIP. Semaglutide also promotes weight loss, but by about 15 per cent on average, suggesting that the added GIP component in tirzepatide gives an extra boost, says Cowley. Like semaglutide, tirzepatide can trigger side effects such as nausea, vomiting, diarrhoea and constipation that seem worse at higher doses. However, doctors’ experience withsemaglutide has revealed that starting patients on low doses and gradually increasing them can avoid these side effects, and the same may be true for tirzepatide, says Joseph Proietto at the University of Melbourne in Australia. One advantage of obesity drugs is that they can be discontinued if necessary, says Proietto. “The downside of bariatric surgery is that you can never ever have a normal meal again, not even for a special occasion,” he says. “With medication, you can still do this.”

Source: https://www.monash.edu/
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https://www.newscientist.com/

How To Regenerate Optic Nerve Cells

Scientists have found a new way to regenerate damaged optic nerve cells taken from mice and grown in a dish. This exciting development could lead to potential eye disease treatments in the future. Damage to full-grown nerve cells causes irreversible and life-altering consequences, because once nerve fibres mature, they lose their ability to regenerate after injury or disease. The new experiments show how activating part of a nerve cell’s regenerative machinery, a protein known as protrudin, could stimulate nerves in the eye to regrow after injury.

With more research, the achievement is a step towards future treatments for glaucoma, a group of eye diseases which cause vision loss by damaging the optic nerve (that links the eye to the brain).

What we’ve seen is the strongest regeneration of any technique we’ve used before,said ophthalmologist Keith Martin from the University of Melbourne in Australia. “In the past it seemed impossible we would be able to regenerate the optic nerve but this research shows the potential of gene therapy to do this.”

In this study, scientists stimulated nerve cells of the eye to produce more protrudin, to see if this would help protect the cells from damage and even repair after injury. First, in optical nerve cells cultured in a dish, the researchers showed that ramping up protrudin production stimulated regeneration of nerve cells that had been cut by a laser. Their spindly axons regenerated over longer distances, and in less time, than untreated cells.  Next, adult mice were administered gene therapy – an injection straight into the eye – carrying instructions for nerve cells to bump up protrudin production. As painful as that sounds, this procedure can actually be done safely in people (the injection, that is, not yet the gene therapy).

A few weeks and one optic nerve injury later, these mice had more surviving nerve cells in their retinas than the control group did. In one final experiment, the scientists used whole retinas from mice removed two weeks after giving them a protrudin boost, to see if this treatment could prevent nerve cells from dying in the first place. The researchers found, three days later, that stimulating protrudin production had been almost “entirely neuroprotective, with these retinas exhibiting no loss of [retinal] neurons,” the researchers wrote in their paper. Usually, about half of retinal neurons removed in this way die within a couple of days.

“Our strategy relies on using gene therapy – an approach already in clinical use – to deliver protrudin into the eye,” said Veselina Petrova, a neuroscience student at the University of Cambridge. “It’s possible our treatment could be further developed as a way of protecting retinal neurons from death, as well as stimulating their axons to regrow.”

Source: https://www.cam.ac.uk/