This review addresses the control exerted by insulin through its receptor on the general metabolism and gene expression in chicken liver and muscle. Compared with mammals, chickens have similar concentrations of circulating insulin, but still maintain high plasma glucose levels. This may be a consequence of the low sensitivity of the chicken to exogenous insulin. In order to determine whether this low sensitivity is the result of differences in insulin receptor signaling between mammals and birds, insulin receptors have been characterized in several chicken tissues and two insulin receptor substrates (IRS-1 and Shc) have been described in liver and muscle. Compared with mammals current knowledge of insulin signaling in birds is incomplete. This is particularly evident when considering the number of isoforms of the components involved in the insulin cascade (IRSs, AKT, ERK and others) many of which may have not been characterized in the chicken. Despite these shortfalls in available data, it appears that insulin signaling in chicken liver is similar to that in mammals, but is unlike that in mammals in muscle. In leg muscle, chickens differ from mammals in the early steps of the insulin signaling cascade (IR, IRS-1 and PI3K) where PI3K activity is about 30-fold greater in the chicken than in the rat. This "constitutive" hyperactivity of PI3K in chicken muscle may over-stimulate a feedback inhibitory pathway described in mammals thereby desensitizing chicken muscle to insulin. (C) 2008 Elsevier Inc. All rights reserved.