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A new study published in the journal eLife revealed that a hormone capable of suppressing food intake and increasing feelings of satiety in mice showed similar results in humans and non-human primates.
A hormone called Lipocalin-2, or LCN2, could be used as a possible treatment for people who are obese and whose natural satiety cues have stopped working.
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LCN2 is mainly produced by bone cells and occurs naturally in mice and humans.
Studies in mice have shown that long-term administration of LCN2 to animals reduces food intake and prevents weight gain, without slowing their metabolism.
“LCN2 acts as a satiety signal after a meal, which causes mice to reduce their food intake, and it does so by affecting the hypothalamus in the brain,” explains lead author Perestra Ioana Petropolo, who was a post researcher. – PhD from Columbia University.
Petropolo, who is also from the University of Irving Medical Center in New York at the time of the study, and is now at the Helmholtz Diabetes Center, Munich, Germany, added: “We wanted to see if LCN2 had similar effects in humans. and if a dose of it were 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 of normal weight, overweight or obese.
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Subjects in each study were given a meal after a full night of fasting until the next morning, and the amount of LCN2 in the blood was studied before and after the meal. The researchers found that in normal-weight subjects, there was an increase in LCN2 levels after a meal, which coincided with their level of satisfaction after eating.
Conversely, in overweight or obese people, LCN2 levels decreased after a meal.
Based on the post-meal response, the researchers classified the subjects as either non-responders or responders.
Non-responders, who did not show an increase in LCN2 after a meal, tended to have greater waist circumference and higher signs of metabolic disease, including body mass index, body fat, increased blood pressure, and increased blood sugar. .
Significantly, however, subjects who lost weight after gastric bypass surgery experienced recovered sensitivity to LCN2, changing their status from non-responder before surgery to responder after.
Taken together, these results reflect those seen in mice and indicate that post-meal loss of LCN2 regulation is a new mechanism contributing to obesity and could be a potential target for weight loss treatments.
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After verifying that LCN2 could travel to the brain, the team discovered whether hormone therapy could reduce food intake and prevent weight gain.
To do this, they treated the monkeys with LCN2 for a week. They observed a 28% decrease in food intake compared to before treatment within a week, and the monkeys also ate 21% less than their saline-only counterparts.
Additionally, after only one week of treatment, measurements of body weight, body fat and blood lipid levels showed a downward trend in treated animals.
Senior author Stavroulla Costini, professor of cellular physiology and biophysics at Columbia University’s Irving Medical Center, concludes, “We have shown that LCN2 travels through the brain, makes its way into the hypothalamus, and disrupts food intake in non-primates. Our results show that the hormone can restrict appetite suppression with minimal toxicity and paves the way for the next level of LCN2 testing for clinical use. “
Source: Science Daily
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