Mặc dù nó không thể cai trị ra rằng một khoảng tín hiệu insulin phát hiện bởi các phòng thí nghiệm nhiều trong các nền văn hóa tế bào ES có thể có kết quả từ Insulin được hấp thụ từ các phương tiện văn hóa, này hiện tượng artifactual là không chịu trách nhiệm duy nhất về các kiểu hình nội tiết quan sát được tuyến tụy của những nền văn hóa | 160 Lumelsky Although it cannot be ruled out that a portion of insulin signal detected by several laboratories in the ES cell cultures could have resulted from insulin absorbed from the culture medium this artifactual phenomenon is unlikely to be solely responsible for the observed pancreatic endocrine phenotype of these cultures. The finding by different independent groups of glucose-stimulated insulin secretion expression of multiple islet genes by RT-PCR alleviation of hyperglycemia in diabetic mice and the insulin promoter-mediated LacZ expression strongly suggest that pancreatic differentiation indeed takes place in these ES cell cultures. The current debate is evidently a reflection of the rapid growth of this still young field. It is also a reflection of the relative inefficiency and the experiment-to-experiment variability of the existing protocols. These issues will certainly be resolved by further technical refinement driven by progress in our understanding of pancreatic development. 8. CONCLUSION Human ES cells have the potential to provide a virtually unlimited supply of functional cells for treatment of different degenerative diseases including type 1 and type 2 diabetes. Recent results suggest that ES cells can be directed to differentiate into pancreatic endocrine hormone producing cells. Furthermore the differentiated cells can self-organize into cell clusters with structure and cellular composition approximating that of pancreatic islets. However before application of ES cell-based technologies to treat diabetes can become a reality a number of serious obstacles such as poor control and inefficiency of pancreatic differentiation apoptosis of the differentiated cell populations and potential tumorigenicity of the cells need to be overcome. Progress in this field will be highly dependent on advances in understanding normal pancreatic development and especially of the instructive signals responsible for commitment to endodermal and pancreatic fate. .
