Prediabetes inverted in mice by deactivating an enzyme

A group of scientists from the University of Utah states, through a study published in Science, succeeded in reversing the state of pre-diabetes in mice by deactivating an enzyme called dihydroceramide desaturase 1 (DES1).

The deactivation of this enzyme leads to a lowering of the total amount of ceramides, a family of lipid molecules, in the body of mice. DES1 thus becomes a useful target for the possible creation of drugs to prevent the state of pre-diabetes, possibly even in humans. This is a therapeutic strategy that is “extraordinarily effective,” as specified by Scott Summers, one of the authors of the study together with David Kelley.

The same researcher underlines the fact that ceramides play a leading role in metabolism. Among other things, the same researchers have discovered that the ceramides trigger in the body a series of mechanisms to conserve fat in the cells but in the long run it can cause a reduced capacity of the same cells to synthesize the glucose and to withdraw them from the bloodstream.

Furthermore, the same ceramides cause an increase in the conservation of fatty acids in the liver, slowing down the turnover. This can be an advantage in the short term or when food is scarce but if the latter is abundant the cells begin to store a lot of fat because they increase the levels of ceramides, which happens in obesity. This condition then leads to insulin resistance and fatty liver disease, as well as to prediabetes.