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Large prospective studies have shown that insulin secretion declines over time in patients with type 2 diabetes (1). This makes treatment of these patients a moving target, i.e., a regimen that works today may not work next year. The cause or causes for the progressive decrease in insulin secretion rates over time remains uncertain, but several possibilities have been proposed including amylin accumulation in β-cells (2), glucotoxicity, lipotoxicity, and glucolipotoxicity. The concept that prolonged hyperglycemia results in impaired insulin secretion (i.e., glucotoxicity) was first proposed by Unger and Grundy (3) and is now generally accepted. Lipotoxicity, defined as inhibition of insulin secretion by elevated plasma levels of free fatty acid (FFA), was also first proposed by Unger (4). It is supported by many in vitro studies but has remained controversial mainly because inhibitory effects of chronically elevated FFA levels on insulin secretion have been difficult to demonstrate in subjects with normal islets (rev. in 5). On the other hand, the combination of chronically elevated plasma glucose and FFA levels (glucolipotoxicity) has been demonstrated to inhibit insulin secretion from normal and abnormal β-cells in vivo (5–7) and in vitro (8).The article by Pascoe et al. (9) supports the …

Does Inhibition of β-Cell Proliferation by Free Fatty Acid in Mice Explain the Progressive Failure of Insulin Secretion in Type 2 Diabetes?