These findings raise the possibility that cilia dysmotility may be a pathway to islet dysfunction and offers a new therapeutic target for human metabolic diseases. Our studies identify cilia motility as a core beta cell function that, when impaired, leads to reduced ability by the beta cell to respond to glucose and to secrete insulin. We show here that, contrary to assumption, islet primary cilia are motile by using the same dynein machinery as classic motile cilia, and that beta cell cilia motility is required for glucose-stimulated calcium influx and insulin release. Defects in ciliary function manifest in metabolic disorders such as obesity and type 2 diabetes in human ciliopathy syndromes ( 21– 23). Islet cells express primary cilia that regulate glucose-stimulated hormone secretion via G protein–coupled receptor (GPCR) and other specialized signaling pathways ( 17– 20). To examine the possibility that primary cilia may have motility and the functional significance of their movement, we used multimodal imaging to study cilia structure and behavior in human and mouse pancreatic islets. These findings suggest that primary cilia microtubules are dynamic and that the structural distinction between primary and motile cilia may not be absolute. Recent three-dimensional (3D) ultrastructural studies have shown that primary cilia architecture can differ extensively from the classic “9 + 0” configuration, owing to microtubule shifts along the length of the cilium that result in outer microtubules rotating into the center of the axoneme ( 14– 16). However, to date, active dynein-driven motility in primary cilia has not been reported. Primary cilia can also exhibit spontaneous fluctuations from internal actin-myosin forces generated at the cell cortex ( 13). In other tissues, primary cilia can bend passively under external forces such as fluid flow ( 9), where cilia mechanosensing regulates cellular homeostasis via ciliary and cytoplasmic i ( 10– 12). There are exceptions to this dichotomous cilia classification, most notably, the embryonic nodal cilia, which are “9 + 0” primary cilia that have both motility and signaling capacity ( 6– 8).