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Research will always bring surprises. A study in this issue presents a fascinating new mechanism for how insulin secretion may be more tied to functional than actual β-cell mass. Olsson and Carlsson (1) found 20–25% of islets in normal rat pancreata immunostained for pimonidazole, a hypoxia marker that accumulates in cells with oxygen levels <10 mmHg. They make a good case that these islets secrete less insulin than “normal” islets, which have oxygen tensions of ∼40 mmHg. When β-cell mass is decreased with partial pancreatectomy, these dormant islets seem to be called into action. Conversely, when β-cell mass is increased with pancreas transplantation, the number of these pimonidazole-stained sleeping islets increases, suggesting that insulin secretion from a population of islets is no longer needed (Fig. 1).This study may be another example of how animal studies can identify important new mechanisms in humans. However, does such a phenomenon exist in humans and how important might it be? What does inactivity of islets mean? In rats, it means that there are islets with reduced blood flow and low oxygen tension that presumably secrete less insulin—but how much less per islet and how much less for a pancreas that may contain islets with varying degrees of inactivation?It is clear that in the face of insulin resistance, glucose levels can be kept in the normal range by …

Sleeping Islets and the Relationship Between β-Cell Mass and Function