Insulin is known to regulate both metabolic and transport functions in the renal proximal tubule. Insulin present in plasma and in glomerular ultrafiltrate is known to be degraded at this nephron site. This paper summarizes what is known about these processes and about the mechanisms by which the actions of insulin and the degradation of insulin are effected in the proximal tubular epithelial cell. Recent studies have characterized the binding of insulin to specific receptors present in the proximal tubular basolateral membrane. Binding of insulin to its receptor in this membrane is thought to initiate events that lead to the phosphorylation of that receptor. Such insulin-stimulated phosphorylation may mediate hormonal action. A possible role for insulin-like growth factor II in the modulation of the actions of insulin has been suggested by observations in the kidney and in nonrenal cells. These findings are integrated into a model characterizing the nature of the interaction of insulin with the renal proximal tubular cell.
Increased proximal tubular cell catalytic iron content: a result, not a mediator of, hypoxia-reoxygenation injury.
