"Evolving consequences in the genesis of failed secretory dynamics on the part of islet Beta cells
indicate a full panorama of induced effects arising primarily from suppression of insulin transcription. In such
an evolving scenario, the subsequent death of beta cells is a true reflection of cellular injury that redefines
glucotoxicity as another aspect of the diabetic state that progresses in line with increased nonoxidative
production of lipotoxins in the added context of a peripheral resistance to insulin action. Type 1 and type 2
diabetic states would constitute integral representations in evolution of a single pathogenetic pathway that
directly implicates an eventual widespread death phenomenon that depletes the islet Beta cell pool as a final
consequence of evolving transcription failure of the hormone. One might therefore link abnormal compensatory
initial increases in insulin secretion as a marker of impaired transcription dynamics of insulin production arising
largely as a direct consequence of progressive failure of insulin secretion and peripheral availability to tissues
ranging from liver to skeletal muscle and heart and brain. It is the consequence of peripheral effective action
of insulin that integrally converts impaired dynamics of insulin secretion to failed insulin transcription and
subsequent widespread depletion of islet Beta cells"