Fig. 22.1 Reduced beta cell mass in type 2 diabetic patients, as compared to non-diabetic controls, although there is a marked inter-subject variability.

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Fig. 22.1 Reduced beta cell mass in type 2 diabetic patients, as compared to non-diabetic controls, although there is a marked inter-subject variability and clear overlap between the two groups (adapted from [21]) The Islets of Langerhans, Islam, Md. Shahidul (Ed.) ISBN: 978-90-481-3270-6, Springer

Fig. 22.2 Isolated type 2 diabetic (T2DM) islets show Increased apoptosis and enhanced caspase-3 and caspase-8 activities in isolated type 2 diabetic (T2DM) islets, as compared to non-diabetic controls. Adapted from [22] The Islets of Langerhans, Islam, Md. Shahidul (Ed.) ISBN: 978-90-481-3270-6, Springer

Fig. 22.3 ATP production and ATP/ADP ratio increase in non-diabetic but not in type 2 diabetic islets following exposure to 3.3–16.7 mmol/l glucose concentration. Adapted from [27] The Islets of Langerhans, Islam, Md. Shahidul (Ed.) ISBN: 978-90-481-3270-6, Springer

Fig. 22.4 A significant induction of genes involved in endoplasmic reticulum stress (BiP and XBP-1t) in isolated type 2 diabetic islets at increased glucose concentration. Adapted from [23] The Islets of Langerhans, Islam, Md. Shahidul (Ed.) ISBN: 978-90-481-3270-6, Springer

Fig. 22.5 Figure demonstrating the increased the amount of insulin granules in type 2 diabetic beta cells that are pre-exposed to metformin (reproduced with modifications from [22]) The Islets of Langerhans, Islam, Md. Shahidul (Ed.) ISBN: 978-90-481-3270-6, Springer