Treat obesity with appetite hormone News Today

  • | Wednesday | 2nd December, 2020

Chennai: With obesity and its related diseases being some of the most common health issues worldwide researchers have now found a new way to tackle the same. According to a study published in eLife a bone-derived hormone that curbs appetite could be used as a potential treatment in people with obesity whose natural signals for feeling full no longer work. The hormone called Lipocalin-2 (LCN2) suppresses food intake and increase the feeling of fullness in mice has shown similar results in humans and non-human primates. The team first analysed data from four different studies of people in the US and Europe who were either normal weight overweight or living with obesity. By contrast in people who were overweight or had obesity LCN2 levels decreased after a meal.

Chennai: With obesity and its related diseases being some of the most common health issues worldwide researchers have now found a new way to tackle the same. According to a study published in eLife a bone-derived hormone that curbs appetite could be used as a potential treatment in people with obesity whose natural signals for feeling full no longer work. The hormone called Lipocalin-2 (LCN2) suppresses food intake and increase the feeling of fullness in mice has shown similar results in humans and non-human primates. Explaining this lead author Peristera-Ioanna Petropoulou said “LCN2 acts as a signal for satiety after a meal leading mice to limit their food intake and it does this by acting on the hypothalamus within the brain. We wanted to see whether LCN2 has similar effects in humans and whether a dose of it would be able to cross the blood-brain barrier”. The team first analysed data from four different studies of people in the US and Europe who were either normal weight overweight or living with obesity. The people in each study were given a meal after an overnight fast and the amount of LCN2 in their blood before and after the meal was studied. The researchers found that in those who were of normal weight there was an increase in LCN2 levels after the meal which coincided with how satisfied they felt after eating. By contrast in people who were overweight or had obesity LCN2 levels decreased after a meal. Based on this post-meal response people were grouped as non-responders or responders.

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