The insulin receptor is a multifunctional protein encoded by a modular gene. Certain discrete domain within the insulin-receptor structure subserve specific functional properties. This organizational model of the insulin receptor predict the existence of divergent signaling pathway facilitating specific bioeffects.
Although insulin play the dominant role in the control of carbohydrates metabolism in human and other vertebrates, it also profoundly affect growth process in animal. Children with diabetes, for e.g., fail to grow even though GH level are normal, whereas infant of diabetic mother with islet hyperplasia and hyper-insulinism are of increased stature. This might not be too surprising considering the structural similarities among insulin, the IGFs, and their receptors. The growth promoting action of insulin are amply documented, and protein catabolism is accelerated in the absence of insulin. Insulin is required for the full anabolic effect of GH an action that may be because insulin, through its action on glucose uptake by muscle, provide the energy substrate necessary for protein synthesis. Insulin also increase the incorporation of amino acid into muscle by an action that is independent on its effect on glucose metabolism. This may result from the direct action of insulin on the transport of amino acid into cell, as well as activation of ribosomal translational capacity, a protein synthesis per second is not dependent on glucose availability or RNA synthesis. Insulin stimulates the growth of immature hypophysectomized rats, but this action is manifest only when the protein-sparing action of insulin is enhanced by the concomitant feeding of a highly carbohydrate diet.
Insulin at a high concentration, as in familial insulin resistance, stimulates general body growth through low-affinity binding to IGF receptor.
Although insulin play the dominant role in the control of carbohydrates metabolism in human and other vertebrates, it also profoundly affect growth process in animal. Children with diabetes, for e.g., fail to grow even though GH level are normal, whereas infant of diabetic mother with islet hyperplasia and hyper-insulinism are of increased stature. This might not be too surprising considering the structural similarities among insulin, the IGFs, and their receptors. The growth promoting action of insulin are amply documented, and protein catabolism is accelerated in the absence of insulin. Insulin is required for the full anabolic effect of GH an action that may be because insulin, through its action on glucose uptake by muscle, provide the energy substrate necessary for protein synthesis. Insulin also increase the incorporation of amino acid into muscle by an action that is independent on its effect on glucose metabolism. This may result from the direct action of insulin on the transport of amino acid into cell, as well as activation of ribosomal translational capacity, a protein synthesis per second is not dependent on glucose availability or RNA synthesis. Insulin stimulates the growth of immature hypophysectomized rats, but this action is manifest only when the protein-sparing action of insulin is enhanced by the concomitant feeding of a highly carbohydrate diet.
Insulin at a high concentration, as in familial insulin resistance, stimulates general body growth through low-affinity binding to IGF receptor.
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