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Interest in regulation of glucose-induced insulin secretion (GSIS) by arachidonic acid (AA) metabolites began in the early 1970s. The metabolite of primary interest has been prostaglandin E2 (PGE2) because it is one of several negative modulators of GSIS yet unique because it is not classified as a hormone, such as epinephrine or somatostatin. Rather, PGE2 is considered an autocoid because it is a substance whose action takes place in the same cell as its synthesis, which in the case of the pancreatic β-cell suggests PGE2 is an endogenous modulator of GSIS. This autocoid, produced via cleavage of AA from phospholipid and further metabolism by cyclooxygenase-2 (COX-2), is the most abundant AA metabolite in the β-cell. The article in this issue of Diabetes by Neuman et al. (1) takes a fresh look at this pathway by focusing on PGE3, an alternate prostaglandin formed when eicosapentaenoic acid (EPA) rather than AA is used as the dominant dietary substrate. (Before reading further, it may be helpful to examine Table 1 of the article by Neuman et al., which identifies the players in this complex lexicon.) Clinical relevance of this consideration of the impact of a diet rich in EPA stems from the fact that this polyunsaturated fatty acid is proposed to be beneficial in chronic conditions such as diabetes.Historically, long before the discovery of prostaglandins, Ebstein (2) reported in 1876 that treatment of his patients with diabetes with oral sodium salicylate reduced urinary glucose levels. It took nearly 100 years for the Nobel prize–winning work of Vane (3) and his colleagues to establish that nonsteroidal anti-inflammatory drugs, such as sodium …

The COX-2/PGE2/EP3/Gi/o/cAMP/GSIS Pathway in the Islet: The Beat Goes On