The Story


Obesity is a condition of fat accumulation in the body which thus increases the weight of a person. There are over 1 crore people per year who are getting obese in India only and 30% of the world’s population. Well, scientists have found a solution. A hormone that can suppress food intake and increase the feeling of fullness in mice has shown similar results in humans and non-human primates says a new study published in eLife. The hormone which plays the key role in this process is called Lipocalin-2 (LCN2), this hormone when used as a treatment affects brain cell which generates the feeling of fullness. The studies have shown that this hormone is generated in bone cells of mice and humans as well. Studies in mice have shown that giving LCN2 to the anwimals 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 München, Munich, Germany. "We wanted to see whether has similar effects in humans and whether a dose of it would be able to cross the blood-brain barrier."

Scientists studied this by performing experiments on four persons having a difference in their overall fat accumulation in their body, normal weight, overweight, and one with the condition of obesity. they performed their experiments by giving a meal after an overnight fast, and the amount of LCN2 in their blood before and after the meal was studied. those who were normal weight have an incresed amount of LCN2 in their body, which coincided with how satisfied they felt after eating, people who were overweight or had obesity, LCN2 levels decreased after a meal. according to meal responses, the researchers divided people into non-responders or responders. Non-responders are the ones who showed no increase in LCN2 after a meal in their, tended to have a larger waist circumference and higher markers of metabolic disease -- including BMI, body fat, increased blood pressure, and increased blood glucose. 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 afterward. Observing these results carefully they just mirror those seen in mice and show that this loss of post-meal LCN2 regulation is a mechanism that contributes to obesity and could be a potential target for weight-loss treatments. After verifying that LCN2 can cross into the brain, the researchers explored whether treatment with the hormone might reduce food intake and prevent weight gain. To do this, they treated monkeys with LCN2 for a week. They saw a 28% decrease in food intake compared with that before treatment within a week, and the monkeys also ate 21% less than their counterparts who were treated only with saline. Moreover, after only one week of treatment, measurements of body weight, body fat, and blood fat levels showed a declining trend in treated animals. "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."