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Semaglutide is the latest in the line of analogues of GLP1, a gut hormone that signals to the pancreas to increase insulin secretion. Semaglutide and all its predecessors are, in effect, weaponised versions of GLP1, and were originally designed as treatments for type 2 diabetes.
Their main superpower is that they survive for far longer in the blood than the GLP1 that occurs naturally in your body, which only has a half-life of two minutes. Earlier approved GLP1 analogues, including Exenatide from AstraZeneca and Liraglutide from Novo Nordisk, required daily injections. In contrast, someone with type 2 diabetes only needs to inject Semaglutide once a week, thus increasing insulin secretion and speeding the uptake of glucose from the blood into muscle and fat.
But wait a minute, what does any of this have to do with weight loss? Well, this is related to another function of GLP1 as a gut hormone.
Our brain needs to know two key pieces of information in order to control food intake. First, it needs to know how much fat we are carrying. Why? Because our fat is our long-term energy store, and is a marker for how long we would survive in the wild without any food.
The second piece of information our brain needs to know is how much and what we are currently eating, or have just eaten. These are short-term signals that come from our gut. Every time we take a mouthful of food, from the moment we begin chewing, until the moment it emerges from the other end, hormones are secreted. The vast majority of these gut hormones, including GLP1, make us feel full when they signal to the brain.
Therefore, a side effect of having a long-acting GLP1 analogue like Semaglutide hanging about, is that it signals to the brain and makes us feel full. What happens when we feel full? We eat less. What happens when we eat less? We lose weight. In fact, clinical trials with Semaglutide have shown that over two years of once-weekly injections, people lose, on average, 15 per cent of their body weight!
