By H. P. F. Koppeschaar, Torsten Tuvemo, Peter Trainer, Philip Zeitler
Read or Download 38th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: Granada, Spain, April 7-8, 2006 (Hormone Research) PDF
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Diabetes is now a big worldwide illness. approximately 123 million humans have diabetes, nearly 2. 10f the worlds inhabitants. of those a hundred and twenty million have variety 2 diabetes. there's a diversity of purposes for the explosion in occurrence of style 2 diabetes, from alterations in way of life and environmental components to complicated results on genetic susceptibility.
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Extra resources for 38th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: Granada, Spain, April 7-8, 2006 (Hormone Research)
1). The underlying molecular mechanisms remain unclear and they seem to differ from those observed in subjects with T2DM. Based on the study by Nielsen and associates, elevated FFA levels play a causal role ; however, there is no experimental human in vivo data to support the belief that insulin-signaling pathways are affected . Many more studies are needed with particular attention focused on the dosing and timing of GH and insulin and the optimal time to obtain a muscle biopsy. It is also likely that newer methods such as gene arrays and proteomics may be important supplements to current assays, which only measure the activity of single proteins.
The evidence shows that cells that are glucose-responsive for insulin release can be produced using differentiation strategies involving a sequence of growth factor-directed steps. However, because of the close association between neural and pancreatic cell types and markers, it is possible that many of the cells produced by these strategies may be more neural than pancreatic. Thus, it is important to replicate the normal developmental pathways that include the sequential expression of appropriate endoderm and pancreatic progenitor markers.
26 Fujikawa T, Oh SH, Pi L, Hatch HM, Shupe T, Petersen BE: Teratoma formation leads to failure of treatment for type I diabetes using embryonic stem cell-derived insulin-producing cells. Am J Pathol 2005; 166: 1781– 1791. 27 Segev H, Fishman B, Ziskind A, Shulman M, Itskovitz-Eldor J: Differentiation of human embryonic stem cells into insulin-producing clusters. Stem Cells 2004;22:265–274. 28 Brolen GK, Heins N, Edsbagge J, Semb H: Signals from the embryonic mouse pancreas induce differentiation of human embryonic stem cells into insulin-producing beta-celllike cells.