There may be a new strategy in the future for treating type 2 diabetes (the most common form, which is unrelated to the immune system, unlike type 1 diabetes), through adipsin, a protein that is produced by adipose cells and performs various metabolic functions but, in higher than normal concentrations seems also to have a protective effect on the pancreas (the gland affected by diabetes). Researchers from Cornell University in New York and Harvard Medical School in Boston are convinced of this, and published the results of their work in the scientific journal Nature Medicine, after having conducted numerous experiments.
With adipsin (in higher doses than normal, like we said) in particular, the researchers were able to achieve a major result, which is currently not offered by traditional therapies: that of protecting pancreas cells from the destruction that is typical of diabetes.
The work of the US researchers went through various phases. First of all, they increased the levels of adipsin in laboratory animals and demonstrated that this increase had a protective effect on pancreatic beta-cells (those that produce insulin) in the long-term, as well as improving glycaemia and the levels of insulin itself (this hormone plays a key role in the use of glucose, i.e. the main source of energy used by cells, which in diabetics becomes defective, or even lacking).
The researchers then extended their experiments, in the lab, to the cells of the human pancreas, and were able to identify the protective mechanism of adipsin. How does it work? In simple terms, we can say that adipsin enhances the activity of a protein called C3a, which in turn preserves the function of beta-cells. In addition, C3a suppresses an enzyme called Dusp26, which can damage these cells.
Having achieved these results, the researchers then contacted the Massachusetts General Hospital in Boston to check the levels of adipsin in 5570 people who had participated in the Framingham Heart Study, a major study (which began in 1948 and is still ongoing) on the population of the town of the same name in Massachusetts. The researchers were thus able to see that the people with higher levels of this protein in their blood did not develop type 2 diabetes as frequently: due to these higher values, the number of cases was reduced by 50%. Furthermore, the researchers showed that the people with higher levels of adipsin also had a greater amount of subcutaneous fat (i.e. fat immediately under the skin), were more sensitive to the action of insulin (and, so to speak, its protective action) and had a lower quantity of visceral fat, which poses a higher risk of the development of cardiovascular and metabolic disorders.
All of this paints a coherent picture in which, obviously, many elements are yet to be confirmed, before we can start to experiment with possible therapies focusing on adipsin (or also the suppression of the Dusp26 enzyme using other methods). However, if the results are achieved, new avenues in the treatment of type 2 diabetes could be explored, and it would be the first time, as we said, that the integrity of beta-cells could be preserved.
