This is not an article but our request for your help. However, we are not interested in your money but in something more valuable – your time.
We are looking for information that will help us move forward and – as we believe – even closer to a functional solution to our common problems. If you find the answer to this question, we will be grateful if you write this information, including the source, in the comments below or send it to our email helpus@piqaso.com.
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PIQASO team
Why do we ask this question?
The pancreas plays an essential role in energy consumption and metabolism. It consists of two functionally and morphologically distinct components: the exocrine and endocrine. The exocrine pancreas is composed of acinar and ductal cells that secrete digestive enzymes. The endocrine pancreas is composed of five different hormone-secreting cell types that include glucagon-secreting α cells, insulin-producing β cells, somatostatin-releasing δ cells, ghrelin-releasing ε cells, and pancreatic polypeptide (PP)-secreting cells. These cells aggregate to form the islets of Langerhans, which are intermingled with the intra-islet microvascular network and play an essential role in regulation of blood glucose levels by directly secreting insulin and glucagon into the bloodstream. Type 1 diabetes (T1D) and type 2 diabetes (T2D) are defined as blood hyperglycemia caused by an absolute or relative deficiency of pancreatic β cells. Autopsy studies have shown deficits in β cell mass in approximately 70~100 and 0~65% in patients with T1D and T2D, respectively (1, 2). Therefore, β cell mass regeneration is a potential therapeutic strategy for recovery of β cell loss in patients with diabetes.
Regeneration of β cells occurs through endogenous regeneration or exogenous supplementation, such as transplantation of cadaveric islets or grafting of new β cells generated from in vitro cell engineering. Recently, numerous strategies and technologies for producing human insulin-secreting cells have emerged, including in vivo stimulation of existing β cell replication, reprogramming of other pancreatic cells to differentiate into β cells, in vitro differentiation of induced pluripotential stem (iPS) cells into new β cells, and generation of human islets from genetically engineered pigs. However, clinical application has remained a challenge. For example, strategies for enhancing replication of residual β cells have been successful in rodent but not in humans. In addition, drugs that stimulated conversion of α cells into β cells in animal experiments did not do so in clinical trials. As such, it is critical to determine the causes for limited success of clinical trials, and to determine possible strategies for improving cell therapy for T1D.
