Longitudinal Dysregulation of Adiponectin and Leptin Following Blast-Induced Polytrauma in a Rat Model

Blast-induced polytrauma (BIPT) is a common injury among military personnel exposed to explosive blasts. It is increasingly recognized as a complex, multisystem disorder that extends beyond neurological damage to include systemic metabolic and inflammatory dysfunction. Adipokines, particularly leptin and adiponectin, are hormones secreted by adipose tissue and are emerging as key mediators in the pathophysiology of traumatic brain injuries. Yet, their long-term dynamics following blast exposure remain unclear. This study investigated the temporal profiles of plasma leptin and adiponectin in a longitudinal rat model of BIPT. Adult male Sprague Dawley rats were subjected to either a single (B) or repeated (BB) blast exposure (20 psi) or served as sham controls. Plasma samples were collected at 24 h, 1 month, 6 months, and 12 months post-exposure, and adipokine levels were measured using Enzyme-linked Immunosorbent Assay. Adiponectin levels exhibited a biphasic response: both B and BB groups showed significant early decrease at 24 h and 1 month compared to sham animals, followed by robust elevation at 6 and 12 months, particularly in the repeated blast group. In contrast, leptin levels remained unchanged acutely but rose significantly at 6 and 12 months post-blast, with the BB group again showing the highest levels. These patterns indicate sustained, exposure-dependent dysregulation of adipokine signaling after blast trauma. The study provides the first longitudinal profile of systemic adipokine responses to BIPT, revealing their potential as accessible biomarkers and therapeutic targets. These findings support a model of chronic metabolic and inflammatory imbalance in BIPT and warrant further investigation in human cohorts and mechanistic studies.