Open AccessHypogonadism induced by surgical stress and brain trauma is reversed by human chorionic gonadotropin in male rats: A potential therapy for surgical and TBI‐induced hypogonadism?
Author(s) -
Geddes Rastafa I.,
Kapoor Amita,
Hayashi Kentaro,
Rauh Ryan,
Wehber Marlyse,
Bongers Quinn,
Jansen Alex D.,
Anderson Icelle M.,
Farquhar Gabrielle,
VadakkadathMeethal Sivan,
Ziegler Toni E.,
Atwood Craig S.
Publication year - 2021
Publication title -
endocrinology, diabetes and metabolism
Language(s) - English
Resource type - Journals
ISSN - 2398-9238
DOI - 10.1002/edm2.239
Subject(s) - medicine , traumatic brain injury , human chorionic gonadotropin , hypogonadotropic hypogonadism , testosterone (patch) , sham surgery , endocrinology , corticosterone , saline , hormone , pathology , alternative medicine , psychiatry
Hypogonadotropic hypogonadism (HH) is an almost universal, yet underappreciated, endocrinological complication of traumatic brain injury (TBI). The goal of this study was to determine whether the developmental hormone human chorionic gonadotropin (hCG) treatment could reverse HH induced by a TBI. Methods Plasma samples were collected at post‐surgery/post‐injury (PSD/PID) days ‐10, 1, 11, 19 and 29 from male Sprague‐Dawley rats (5‐ to 6‐month‐old) that had undergone a Sham surgery (craniectomy alone) or CCI injury (craniectomy + bilateral moderate‐to‐severe CCI injury) and treatment with saline or hCG (400 IU/kg; i.m.) every other day. Results Both Sham and CCI injury significantly decreased circulating testosterone (T), 11‐deoxycorticosterone (11‐DOC) and corticosterone concentrations to a similar extent (79.1% vs. 80.0%; 46.6% vs. 48.4%; 56.2% vs. 32.5%; respectively) by PSD/PID 1. hCG treatment returned circulating T to baseline concentrations by PSD/PID 1 (8.9 ± 1.5 ng/ml and 8.3 ± 1.9 ng/ml; respectively) and was maintained through PSD/PID 29. hCG treatment significantly, but transiently, increased circulating progesterone (P 4 ) ~3‐fold (30.2 ± 10.5 ng/ml and 24.2 ± 5.8 ng/ml) above that of baseline concentrations on PSD 1 and PID 1, respectively. hCG treatment did not reverse hypoadrenalism following either procedure. Conclusions Together, these data indicate that (1) craniectomy is sufficient to induce persistent hypogonadism and hypoadrenalism, (2) hCG can reverse hypogonadism induced by a craniectomy or craniectomy +CCI injury, suggesting that (3) craniectomy and CCI injury induce a persistent hypogonadism by decreasing hypothalamic and/or pituitary function rather than testicular function in male rats. The potential role of hCG as a cheap, safe and readily available treatment for reversing surgery or TBI‐induced hypogonadism is discussed.