Lipid transport by TMEM24 at ER–plasma membrane contacts regulates pulsatile insulin secretion

Understanding insulin release Insulin release takes place in two phases: a first rapid burst followed by a series of small exocytic bursts that coincide with pulsatile spikes in cytosolic Ca 2+ levels. The second phase is impaired in patients with type II diabetes, underscoring the importance of understanding its molecular basis. Lees et al. report a mechanism through which TMEM24, a lipid transport protein that concentrates at endoplasmic reticulum–plasma membrane contact sites, regulates the pulsatility of cytosolic Ca 2+ and phosphoinositide signaling. This process in turn regulates pulsatile insulin secretion during the slow insulin release phase. Science , this issue p. eaah6171