During an experiment, research leader Dr. Stephan Herzig and his colleagues switched off the cortisol receptor in the livers of mice, which led to a considerable decline in the levels of fat in the animals' livers.
Upon further investigation, the researchers observed that the experimental mice's livers started producing large amounts of a protein called HES1 in the absence of the cortisol receptor.
HES1 activates a number of enzymes that break down fat and, thus, counteract fat accumulation in the liver.
The research team say that the mice that were treated with cortisol showed a decline in HES1 levels and a rise in the accumulation of fat in their livers.
Based on their observations, the researchers came to the conclusion that the cortisol receptor acts as a switch that puts the HES1 gene off completely.
"We have discovered a key mechanism here that plays a crucial role in many pathologic metabolic disorders. It has been obvious for some time that there is an association between the body's own cortisol or therapeutically administered cortisone and the development of fatty liver. Now we also know what the interconnections look like at a molecular level," says Stephan Herzig.
This finding attains significance because fatty liver can give rise to many metabolic diseases, such as the metabolic syndrome known as "deadly quartet".
Furthermore, a combination of fatty liver, obesity, diabetes, and hypertension is regarded as the primary cause of life-threatening vascular events such as myocardial infarction and stroke.