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2 Mechanisms producing lesion and regeneration of pancreatic islets
The proliferation capacity of adult beta cells is very low A system enabling selecting the beta cells which are proliferating has been developed, based on incorporating EdU and its later puri cation by means of ow cytometry (Carballar et al , Sci Rep 2017)
3 Preventive and therapeutic strategies in regenerative medicine, cell therapy and
gene therapy
The conditional suppression of Jarid2 in pancreatic progenitors reduces the area of endocrine cells at the time of birth This is due to a prenatal alteration, in the process of di erentiation and proliferation of those cells The role of Jarid2 occurs after endocrine di erentiation Jarid2 is necessary to complete the activation of the beta cell di erentiation programme, which means that their manipulation can be used for improving protocols for obtaining beta cells from stem cells (Cervantes et al , Sci Rep 2017)
A platform has been created for cell culture based on self-assembling peptide nano bres (RAD16-I), functionalised with extra-cellular matrix peptides for the redi erentiation and generation of insulin-pro- ducing cells which could be used in diabetes cell therapy (Aloy-Reverté, Tissue Engineering: Part A, 2017)
Lastly, an Investigational Medicinal Product has been developed, with the aim of using insulin-producing cells obtained from human embryonic stem cells in clinical trials
Cell and molecular mechanisms involved in the development and progression of diabetes type 2 and identi cation of new therapeutic targets
Coordinator: Antonio Zorzano Olarte
1 Determinants of insulin resistance: molecular mechanisms involved
It has been proven that alterations in methylation and expression of genes involved in the regulation of energy homeostasis are related with foetal growth and neonatal corporal composition and could be among the rst mechanisms modulating later susceptibility to diabetes (Díaz et al , Diabetes 2017)
Apart from this new mechanism by means of which PPARβ/δ and FGF21 regulate levels of VLDL re- ceptors and in uence the development of hepatic steatosis have been described (Zarei et al , Mol Metab 2017) It has also been shown that VLDL particles and apolipoprotein C-III induce reticulum stress and in ammation and attenuate insulin signalling through the TLR2–like receptor in mouse skeletal muscle cells (Botteri et al , Diabetología 2017)
It has also been proven that there is a need for intact MTORC1 signalling to regulate two processes re- quired for elimination of damaged mitochondria, i e in what represents the start of general autophagy and targeting uncoupled mitochondria to the autophagic machinery through PINK1/Parkin proteins (Bar- tolomé et al , Mol Cell Biol 2017)