In patients with type 2 diabetes, plasma glucose levels are elevated; and consequently, fasting plasma insulin. Although the insulin levels sometimes increase slightly after a meal in patients with type 2 diabetes mellitus this is considerably less than normal. In studies in which glucose levels have been raised by glucose infusions (hyperglycemic clamps) to comparable levels in diabetic subjects and controls, it has become clear that second-phase insulin secretion is roughly 25% (IGT) to 50% decreased in type 2 diabetes (53). First-phase secretion is generally completely lost. In normoglycemic first-degree relatives insulin secretion is also diminished but to a lower extent, presumably on a genetic basis (54). It is suspected that upon acquaintance of insulin resistance (obesity, physical inactivity) the pancreas that has already lower secretory capabilities can adapt less than normal, which might lead to decreased glucose tolerance or diabetes. It has been widely suggested that various mechanisms might further
aggravate beta-cell insulin secretory dysfunction, among which glucose toxicity, lipotoxicity, and amyloid deposition.
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