The regulation of the sugar and lipid balance in the body is a vital function of the liver: In times without food intake, the liver produces glucose, a sugar, but quits producing glucose right after a meal, since glucose can now be obtained from the food in the bowels. The signal that makes the liver quit the release of glucose originates in the pancreas, i.e. the insulin hormone. Upon the manifestation of a diabetic disease, this signal is too late and reduced in intensity, which may result in a high blood sugar level after a meal. Scientists from the Helmholtz Centre for Infection Research (HZI) and the Braunschweig Integrated Centre of Systems Biology (BRICS) investigated these relationships with a mathematical model of liver cells and found that not only the overall quantity of the insulin signal, but the fact that insulin is released to the liver in a pulsatile manner is crucial. Infections or systemic inflammations afflicting the pancreas may change this and thereby cause the first symptoms of diabetes. The scientists published their results in Nature Communications. Involved BRICS research group: Systems-Immunology.
