Diabetes mellitus is often presented to people as a disease resulting from improper life choices, such as low levels of physical activity and excessive eating of sugary foods – however, this is far from always the cause of diabetes. So today, a team of specialists from the University of California presented the results of their new study, according to which increased insulin secretion by pancreatic cells can be triggered by an external mechanism, in addition to beta cells in the liver. And experts have demonstrated the viability of their theory with laboratory tests.
Tests were performed on mice induced by the pre-diabetes state and on human living cells to illustrate a possible difference in this mechanism. At first, they managed to conduct a closed test, during which human cells actually began to increase insulin resistance using endogenous beta cells, but then scientists added the so-called fatty acids to the experiment and observed the process again.
It turned out that fatty acids in large quantities can also become a trigger for the onset and development of type 2 diabetes mellitus, both in humans and in experimental mice. In particular, they noticed that an increase in the level of fatty acids is likely to trigger an increased release of a protein called cyclophilin D, which, in turn, begins to affect liver cells, causing them to progressively increase the level of resistance of cells to insulin and also increase the level of blood glucose.
Thus, the presented new mechanism of diabetes mellitus can well be considered as a real threat, since the level of consumption of fatty acids among the majority of the healthy population of the world is significantly higher than the consumption of glucose-containing substances and products. Therefore, the illustrated result can be quite eloquent and detailed in relation to the consideration of hidden triggers and mechanisms of this disease.