Osteoblasts against obesity

Hormone that turns off the feeling of hunger may help in the treatment of obesity

Tatiana Matveeva, "Scientific Russia"

The hormone lipocalin-2, which can increase the feeling of satiety in mice, also works in primates, according to a new study by American scientists. The results published in the journal eLife (Petropoulou et al., Lipocalin-2 is an anorexigenic signal in primates) show that this hormone can be used as a potential treatment for obesity. The news appeared on the website of eLife magazine (Hormone found to switch off hunger could help tackle obesity).

Lipocalin-2 (LCN2) is mainly produced by bone cells (osteoblasts) and is naturally found in mice and humans. In a study on mice, scientists injected LCN2 into rodents for a long time. As a result, the mice decreased the need for food, the mice stopped gaining weight. At the same time, the metabolism has not changed. 

Further, the authors of the work found out whether this hormone has the same effect on people. First, they analyzed data from four different studies of people in the United States and Europe who were normal weight, overweight or obese. In each study, subjects were given food after a night of fasting and the amount of LCN2 in their blood was studied before and after eating. The researchers found that people with normal weight had higher levels of LCN2 after eating, which coincided with their feeling of fullness. 

On the contrary, in overweight or obese people, the level of LCN2 decreased after eating. Based on this reaction after eating, the researchers divided people into two groups: those who can respond to treatment, and those who do not respond. Those who did not respond to treatment – those who did not increase the hormone LCN2 after eating – tended to have higher markers of metabolic diseases: high body mass index, high blood pressure and elevated blood glucose levels. It is noteworthy, however, that in people who lost weight after bypass gastric anastomosis (a surgical procedure for weight loss), sensitivity to LCN2 was restored. 

Adding up the results observed in mice and in humans, the scientists suggested that this loss of LCN2 regulation after eating is a novel mechanism contributing to obesity and could be a potential target for the treatment of obesity.

After making sure that LCN2 could enter the brain, the team conducted preclinical trials and tested whether hormone treatment could reduce food intake and prevent weight gain. For a week, scientists treated non-human monkeys with LCN2. They saw a 28% reduction in food intake compared to what it was before treatment, and the monkeys also ate 21% less than their counterparts who received saline. Moreover, after just one week of treatment, measurements of body weight, body fat and blood fat levels showed a downward trend in treated animals.

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