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Washington [US]Nov. 28 (ANI): In recent research, scientists found that a hormone capable of suppressing food intake and increasing feelings of satiety in mice showed similar results in humans and non-human primates.
The study was published in the journal eLife.
The hormone, called Lipocalin-2 (LCN2), could be used as a potential treatment in people with obesity whose natural cues to feel full no longer work.
LCN2 is mainly produced by bone cells and occurs naturally in mice and humans. Studies in mice have shown that giving LCN2 to animals over the long term reduces their food intake and prevents weight gain, without leading to a slowing of their metabolism.
“LCN2 acts as a signal for satiety after a meal, leading mice to limit their food intake, and it does so by acting on the hypothalamus within the brain,” explains lead author Peristera-Ioanna Petropoulou, who was a postdoctoral researcher at Columbia University Irving Medical Center, New York, USA, at the time the study was conducted and is now located at the Helmholtz Diabetes Center, Helmholtz Zentrum Munchen, Munich, Germany. “We wanted to see if LCN2 has similar effects in humans and if a dose of it would be able to cross the blood-brain barrier.” The team first analyzed data from four different studies of people in the United States and Europe who were either normal weight, overweight, or living with obesity. People in each study received 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.
Conversely, in overweight or obese people, 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 sugar. Surprisingly, however, people who had lost weight after gastric bypass surgery were shown to have restored sensitivity to LCN2, changing their status from non-responder before surgery to responder 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.
After verifying that LCN2 can cross the brain, the team looked into whether treatment with the hormone could reduce food intake and prevent weight gain. To do this, they treated the monkeys with LCN2 for a week. They saw a 28% decrease in food intake compared to that before treatment within a week, and the monkeys also ate 21% less than their counterparts who had been treated with saline only. Furthermore, after only one week of treatment, measurements of body weight, body fat and blood fat levels showed a tendency to decline in treated animals.
“We have shown that LCN2 crosses the brain, travels to the hypothalamus and suppresses food intake in non-human primates,” concludes senior author Stavroula Kousteni, professor of cellular physiology and biophysics at Columbia University Irving Medical Center. “Our results show that the hormone can curb appetite with negligible toxicity and lay the foundation for the next level of LCN2 testing for clinical use.” (ANI)
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