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Yeda R&D Co. Ltd
Abstract ID: 1610
In healthy individuals, Insulin is produced by beta cells of the pancreas. In people with type 1 diabetes mellitus (T1DM), these cells do not produce enough Insulin to
In healthy individuals, Insulin is produced by beta cells of the pancreas. In people with type 1 diabetes mellitus (T1DM), these cells do not produce enough Insulin to effectively fine-tune blood sugar levels. In the US alone there are up to 3 million affected individuals with 30,000 new cases diagnosed each year. Worldwide, T1DM incidence has been increasing in recent years by 2% to 5%. Traditionally treated by multiple daily injections of recombinant Insulin, T1DM management represents a significant burden to both patients and the healthcare system. Recent data estimate that T1DM costs the US ~$15 billion annually in medical costs and lost income.
Thus, novel therapeutic approaches to amplify Insulin production in diseased beta cells or to replace them entirely are in great need.
A research team headed by Dr. Hornstein from the Weizmann Institute has discovered an essential role for microRNA-7 (miR-7), a microRNA that is highly and selectively expressed in the endocrine pancreas, in the regulation of beta cell differentiation. By down-regulating the expression of miR-7, the researchers were able to accelerate beta cell differentiation, and concomitantly to augment their Insulin production rate. The data gained from these studies can be further utilized in cell-based therapy applications to restore Insulin production in damaged beta cells, or alternately to replace these cells with stem cells coaxed to differentiate towards a beta cell fate.
The present technology describes a cell-based method to enhance beta cell differentiation and Insulin production by the downregulation of a pancreas-enriched microRNA.
Please enquire quoting reference no. 1610 regarding licensing or codevelopment partnerships.
Last Updated May 2015