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Circulating glucose levels serve as the principalregulator of the rate of insulin secretion fromthe pancreatic b-cell, which, in turn, is the body’sprincipal mechanism preventing excessive ele-vation in circulating glucose. The control center for this critical negative feedback loop is generally thought to reside solely within the province of the b-cell. However, in the February issue of Diabetes, Osundiji et al. (1) provide evi-dence that there may be another player involved, namely, the hypothalamus. They observed that raising glucose levels locally or pharmacologically blocking glucose entry into cells close to the third ventricle of the rat altered the acute insulin secretory response to intravenous glucose, pre-sumably by the extensive neural connections that exist between the hypothalamus and islet. As pointed out by the authors, it is now well recognized that a subgroup of hypothalamic neurons, and neurons elsewhere in the brain, have the capacity to sense glucose and influence the se-
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Chan et al. (2012) studied this question.
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