ABSTRACT Background: Traumatic brain injury (TBI) is frequently accompanied by neuroendocrine disturbances involving the hypothalamic–pituitary–thyroid (HPT) axis and vitamin D–calcium– phosphorus homeostasis. Despite increasing interest in nutritional strategies after TBI, the effects of branched-chain amino acid (BCAA) supplementation on post-injury neuroendocrine homeostasis, including thyroid hormone levels, vitamin D status, and calcium–phosphorus balance, remain insufficiently characterized. Methods: Twenty-eight male Wistar rats were randomly assigned to Control, Sham, TBI, and TBI + BCAA groups. Moderate TBI was induced using a closed-head weight-drop model. BCAA (0.26 g/kg) was administered orally after injury. Motor function was assessed using balance beam and gait analysis, and serum levels of thyroid hormones, 25-hydroxyvitamin D, calcium, and phosphorus were measured. Results: TBI induced a negative body weight change, impaired balance and gait, reduced serum thyroid hormones, 25-hydroxyvitamin D, calcium, and phosphorus levels, and decreased brain and hippocampal morphometric parameters. Post-injury BCAA supplementation significantly attenuated TBI-associated body weight loss and improved balance beam scores and gait parameters relative to the untreated TBI group. In addition, BCAA treatment partially restored serum thyroid hormones, 25-hydroxyvitamin D, calcium, and phosphorus levels, although values did not fully return to control levels. BCAA supplementation also partially attenuated TBI-induced changes in gross brain and hippocampal morphometric parameters. Conclusion: Post-injury BCAA supplementation exerted modulatory effects, as reflected by partial improvement in neuroendocrine parameters and motor performance. However, incomplete ACCEPTED MANUSCRIPT ARTICLE IN PRESS ARTICLE IN PRESS normalization indicates that BCAA supplementation supports metabolic and functional adaptation rather than full endocrine or structural recovery. These findings suggest that BCAAs may serve as a complementary nutritional strategy to mitigate post-TBI neuroendocrine dysfunction.
