The researchers found increased LCN2 levels in people of normal weight and decreased levels in those who were overweight or obese. Based on levels, the participants were grouped as responders (higher levels) and nonresponders (no increase in LCN2 levels).
Nonresponders, 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.
Researchers also found that people who had lost weight after gastric bypass surgery had a restored sensitivity to LCN2 — changing their status from nonresponders before their surgery, to responders afterward.
After verifying that LCN2 can cross into the brain, the team 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.”