The are approx. 177 million people suffering from diabetes worldwide and this number will be doubled by 2030. Patients with type 1 diabetes require multiple injections of insulin daily with doses careful adjusted on carbohydrate intake, level of activity and stress. Often there is a mismatch between insulin requirements and the calculated dose, resulting in hyper or hypoglycaemia. Between 20-30% of patients however suffer from recurrent hypoglycaemia, which may require third party help (Geddes et al. 2008). Islet transplantation has been a promising therapy since the "Edmonton protocol" was published in 2000 (Shapiro et al. 2000). However, numbers of transplants remain low for a variety of reasons (Shapiro et al. 2006). One major hurdle to more widespread provision of this treatment remains a shortage of supply of donor organs, with only 25-30% of isolations resulting in islets of sufficient quantity and quality to be used in clinical transplantation, indicating a huge waste of valuable resources (Nano et al. 2005). Studies using animal models have found the evidences of neogenisis of beta cells under non-physiological condition as well the limited proliferation capacity of beta cells. Unfortunately, human beings cannot be manipulated to generate insulin-producing cells. There are increasing evidence suggested that glucose response insulin-producing cells could be generated in large quantity for human use. The following are a few possible aspects that can be explored for this purpose. 1.1 Beta cell replication and regeneration There are substantial evidences suggesting that the adult pancreas can generate new-cells in response to pancreatic damage or increased demand for insulin (Wang et al., 1995; Bonner-Weir et al., 1993; Guz et al., 2001). The source of new-cells is thought to be the replication of existing-cells under normal growth condition (Dor et al., 2004). However, the capacity of mature-cells to proliferation and then re-differentiate back into-cells has not been demonstrated in vitro and it still remains a challenge. In addition to the replication, there are mounting evidences indicated that regeneration of beta cells also contribute significantly to the new beta cells when pancreas is under non-physiological conditions such as partial pancreas duct ligation (Wang et al., 1995) or partial pancreatectomy (Finegood et al., 1999). However, such mechanisms are believed to have little implication to diabetes patients, as it is not possible to mimic the situations in animals to humans. Furthermore,
