By now you are probably aware just how horrible obesity can be for your health. Not only can it put you at the risk of ailments like heart disease and diabetes—but it can also put you on the war path of covid-19. No wonder then, the medical community has been looking for solutions to help people manage this problem.
One of the latest advents from the medical community have come in the form of a hormone that can suppress appetite and thus help control obesity.
The hormone, called Lipocalin-2 (LCN2), could be used as a potential treatment in people with obesity whose natural signals for feeling full no longer work. The findings of the study that discovered the hormone were published in the journal eLife.
LCN2 is mainly produced by bone cells and is found naturally in mice and humans. Studies in mice have shown that giving LCN2 to the animals long term reduces their food intake and prevents weight gain, without leading to a slow-down in their metabolism.
“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,” explains lead author Peristera-Ioanna Petropoulou, who was a Postdoctoral Research Scientist at Columbia University Irving Medical Center, New York, US, at the time the study was carried out and is now at the Helmholtz Diabetes Center, Helmholtz Zentrum Munchen, Munich, Germany.
“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.”
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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, the researchers grouped people as non-responders or responders. Non-responders, who showed no increase in LCN2 after a meal, tended to have a larger waist circumference and higher markers of metabolic disease—including BMI, body fat, increased blood pressure and increased blood glucose.
Remarkably, however, people who had lost weight after gastric bypass surgery were found to have a restored sensitivity to LCN2—changing their status from non-responders before their surgery, to responders afterwards.
Taken together, these results mirror those seen in mice and suggest that this loss of post-meal LCN2 regulation is a new mechanism contributing to obesity and could be a potential target for weight-loss treatments.
“We have shown that LCN2 crosses to the brain, makes its way to the hypothalamus and suppresses food intake in non-human primates,” concludes senior author Stavroula Kousteni, Professor of Physiology and Cellular Biophysics at Columbia University Irving Medical Center.
“Our results show that the hormone can curb appetite with negligible toxicity and lay the groundwork for the next level of LCN2 testing for clinical use,” he added.
(With inputs from ANI)