FUNCTIONAL CHANGES OF MICE PANCREATIC ISLETS AS A GUIDE TO IMPROVE BETA-CELL DERIVED FROM HUMAN PLURIPOTENT STEM CELLS MATURATION.

Diabetes Mellitus (DM) is a metabolic syndrome characterized by chronic hyperglycemia. Regardless of its etiology, the pathophysiology of DM lies in the reduction of functional pancreatic β cell numbers, so any type of DM would be benefited from a treatment that promotes β cell replacement. One promising technique is the development of β cell derived from human pluripotent stem cells (hPSC-β). The limiting factor of this approach is the viable generation of hPCS- β necessary for human transplantation, due to the inability to reach a maturation state enough to secrete insulin, and so, being unable to reverse the DM state. In order to develop strategies that reach hPSC-β maturation, it is essential to comprehend how the maturation process occurs throughout its development and point the elements and all possible factors involved. It is known that glucose-stimulated insulin secretion capacity would be achieved due to alterations in transcription factors, AMPK and mTOR pathways, mitochondrial activity, and in the insulin processing machinery and its exocytosis during maturation.