Chronic lipid loading in pancreatic beta-cells of young and old animals causes the intensification of secretion the morphologic equivalents of which are revealed by elevation of number and sizes of mitochondria, granular endoplasmatic reticulum and Golgi apparatus of beta-cells with the quantitative increase of intraorganelle ultrastructures and decrease of volume share and number of secretor granules, which are more prominent in old animals. After definitive period following the chronic lipid loading the secretor processes in young age are normalized (organelles turn back to their initial volume state and consist of the same initial number of intraultrastructures), whereas in old age -- are markedly lower compared with the norm (size and number of organelles and their inner structures are decreased; volume part of secretory granules is increased); in some part of beta-cells complete block of secretion takes place (in the part of beta-cells the irreversible changes are developed; stagnation of secrete is prominent). Therefore any metabolic disease or syndrome running on the background of chronic lipidemia, seems to be a risk-factor for development of Diabetes Mellitus in organisms of old age.