Cross-talk between insulin resistance and nitrogen species in hypoxia leads to deterioration of tissue and homeostasis.

Abstract

Hypoxia has been linked with insulin resistance as it produces changes in the metabolism of the cell; in which the adipocytes impede the insulin receptor tyrosine, phosphorylation, directing at decreased levels of transport of glucose. At this juncture, we are focusing on cross-talk between insulin resistance and nitrogen species in hypoxia, leading to the deterioration of tissue and homeostasis. Physiological levels of nitric oxide play a very crucial role in acting as a priority effector and signaling molecule, arbitrating the body's responses to hypoxia. Both ROS and RNS are associated with a reduction in IRS1 phosphorylation in tyrosine, which leads to reduced levels of IRS1 content and insulin response, which further leads to insulin resistance. Cellular hypoxia is a trigger to inflammatory mediators which signal tissue impairment and initiate survival requirements. But, hypoxia-mediated inflammation act as a protective role by an immune response and promotes wound healing during infection. In this review, we abridge the crosstalk between the inflammation and highlight the dysregulation in physiological consequences due to diabetes mellitus. Finally, we review various treatments available for its related physiological complications.