Insulin is the body's major anabolic hormone. Its secretion and action govern tissue accretion of carbohydrate, fat, and protein, the hallmarks of growth. Insulin's customary site of synthesis, the beta-cells of pancreatic islets which are surrounded anatomically by the digestive juices of the exocrine pancreas, places it strategically in close proximity to the nutrient absorption ultimately essential for growth. In general, provided insulin action is not impaired, excessive insulin secretion whether secondary to excessive nutrient intake or primary as a result of islet cell hyperplasia results in excessive growth (Table 1). In contrast, severe deficiency of insulin secretion or of its action at the receptor or post-receptor step is invariably associated with poor growth in utero as well as postnatally. Some of insulin's growth-promoting effects on carbohydrate and fat may be facilitated by other hormones such as glucocorticoids which simultaneously oppose insulin's protein anabolic effects, whereas growth hormone and sex steroids, especially testosterone, facilitate insulin's protein anabolic actions while countering its effects on carbohydrate and fat. The pivotal role of insulin in growth is further substantiated by the fact that the effects of growth hormone on growth are thought to be mediated indirectly by the generation of somatomedins, also known as insulin-like growth factors (IGFs), which act in an autocrine, paracrine, or endocrine manner to promote growth. Among these, IGF-I is a growth hormone–dependent but probably also insulin-dependent factor. This article reviews the physiologic, biochemical, and molecular basis of insulin action as a growth factor. It also reviews clinical situations in which excessive insulin secretion is associated with excessive growth even in the absence of growth hormone, whereas impaired insulin secretion or action is associated with poor growth even in the presence of excessive growth hormone.