Published online Jan 21, 2019. doi: 10.5527/wjn.v8.i1.11
Peer-review started: September 28, 2018
First decision: October 26, 2018
Revised: November 15, 2018
Accepted: December 10, 2018
Article in press: December 10, 2018
Published online: January 21, 2019
Insulin is an important hormone that affects various metabolic processes, including kidney function. Impairment in insulin’s action leads to insulin resistance in the target tissue. Besides defects in post-receptor insulin signaling, impairment at the receptor level could significantly affect insulin sensitivity of the target tissue. The kidney is a known target of insulin; however, whether the kidney develops “insulin resistance” is debatable. Regulation of the insulin receptor (IR) expression and its function is very well studied in major metabolic tissues like liver, skeletal muscles, and adipose tissue. The physiological relevance of IRs in the kidney has recently begun to be clarified. The credit goes to studies that showed a wide distribution of IR throughout the nephron segments and their reduced expression in the insulin resistance state. Moreover, altered renal and systemic metabolism observed in mice with targeted deletion of the IR from various epithelial cells of the kidney has strengthened this proposition. In this review, we recapitulate the crucial findings from literature that have expanded our knowledge regarding the significance of the renal IR in normal- and insulin-resistance states.
Core tip: Dysregulation of the renal insulin receptor (IR) not only affects local renal metabolism, but also disturbs the systemic glucose homeostasis and blood pressure, leading to metabolic abnormalities. The objective of this review is to highlight the pathophysiological stature of renal IRs in the kidney function, as well as, overall metabolism.