This article was published in Nature Communications, a highly prestigious and influential journal, which amply demonstrates the quality of the research. The peer review process for this journal, in which I have also published in the past, is very strict and rigorous, meaning that the research had to undergo quality scrutiny that confirms that its results are more than valid and support the conclusions of the study. On a personal level, and as an expert in the specific field of brown adipose tissue secretion, I agree and believe that the work is indeed of high scientific quality and includes multiple experimental models that lead to solid and reliable conclusions.

Recent international studies in humans have shown that people with more brown adipose tissue have a lower risk of developing type 2 diabetes or cardiovascular disease, something that has also been extensively demonstrated in the scientific literature in animal models. Due to the relatively small amount of active brown adipose tissue, especially in humans, the general consensus is that this metabolic protection is not so much due to the special ability of brown adipose tissue to burn fat and generate heat per se, but rather to how it “talks” to other cells to coordinate this metabolic improvement. In other words, the ability of activated brown adipose tissue to release substances that either act on themselves, promoting their activation, such as neuritin-1, or, as a result of this activation, also produce other substances that act as hormones, which are released into the blood to communicate with distant organs (called “batoquins”). Of particular interest is the possibility of communication between brown adipose tissue and white adipose tissue, that is, the fat deposits that accumulate in overweight and obese individuals, thus giving the brown fat the order to mobilize its reserves to be burned and thus reduce our weight and blood lipid and sugar levels to prevent or counteract obesity, type 2 diabetes, cardiovascular disease, or fatty liver.

This discovery reveals for the first time an interesting new mechanism by which brown adipose tissue can be activated; it even shows that treatment with neuritin-1 of brown adipose tissue cells is sufficient to activate their “fat-burning” function in experimental models. Activating it in adult humans would not only contribute to direct fat burning, but also increase communication between brown adipose tissue and other organs through the release of batokines. Knowing this mechanism, new therapeutic strategies could be designed that target it to activate brown adipose tissue and improve the metabolic status and quality of life of people living with obesity, diabetes, or fatty liver disease.

The main limitation, which is also echoed in the article and press release, is that this is a study conducted in experimental models (cells and animals). In the case of adult humans, we have less brown adipose tissue than mice in relation to our size, which also becomes progressively inactive with age and especially in conditions of obesity or diabetes. To verify that this molecule is effectively performing the same actions as in experimental models and its causal association with obesity or diabetes, it would be necessary to check its regulation and blood levels in both healthy humans and those with these clinical conditions. In turn, even if human neuritin-1 did indeed perform these actions, as it is a protein that must maintain its complex structure in order to perform its functions, it would be difficult to market it as such in an injectable form, for example, so the strategy to be followed would be to finish discovering exactly how it acts in brown adipose tissue cells and design a drug that simulates its actions.