7^th Indo Global Diabetes Summit and Medicare Expo

Biography

Biography: Vijayalakshmi V

Abstract

Diabetes is characterized by near (type 1) or relative (type 2) deficiency and the regulation of β-cell mass is a critical issue in understanding the disease, when pancreatic islet regeneration can compensate the loss of functional β-cells and forms an attractive strategy for the control of diabetes. Working in this direction , we have demonstrated for the expansion and differentiation of the pancreatic progenitors such as Ductal epithelial cells(DEC)/CK-19+ve/ABCG-2 /PLP and Nestin positive cells (NPC) / ABCG-2 / RA in a STZ induced diabetic mice model system under the nutrient regulation of PLP/Vitamin B6 and all Trans Retinoic acid.The in vitro generated neoislets were functionally viable, and three weeks of post Tx almost normalized the hyperglycemic response, upregulation of key transcription factors (Pdx-1,Glu-2 and Reg, Insulin) vis a vis evidences of beta cell regeneration. Yet in another approach studies by Vikas etal (2009) and kadam et al (2011) have well documented for the differentiation potential of MSCs (adipose /& and placenta ) to generate ILCCS ,and their ability to reverse hyperglycemia in model system.Their findings are significant keeping in view that Mesenchymal stem cells (perinatal tissues,adipose derived ,Bone marrow) display remarkable immunomodulatory, reparative and anti-inflammatory properties and studies show that they augment repair process by secreting paracrine factors to modulate the milieu.With the advent of iPSCs technology, to recreate physiological milieu using adult stem cells to generate embryonic like stem cells / and their differentiation to ILCCS hold further promises of stem cells in the management of diabetes in future.