(781.4) Distinct Effects of Mesterolone on Oxidative and Glycolytic Fibers of Avian Skeletal Muscle

Poster Board Number: C49
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Odd poster #s – 10:15 am – 11:15 am
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Mohammed Allouh (College of Medicine and Health Sciences, United Arab Emirates University), Zakaria Ouda (College of Medicine and Health Sciences, United Arab Emirates University), Sara Ouda (College of Medicine and Health Sciences, United Arab Emirates University)

Aim: Oxidative and glycolytic muscle fibers differ in their responses to physiological stimuli and pathological insults. We examined whether these fibers respond differentially to exogenous anabolic androgenic steroids (AASs) by comparing morphological and histological changes between the oxidative anterior latissimus dorsi (ALD) and glycolytic pectoralis major (PM) fibers in adult avian muscles.

Methods: The AAS mesterolone was selected for this study. Mesterolone is a synthetic steroid that has no estrogenic side effects, low hepatotoxicity, and confers oral activity that allows its oral route of administration. Adult female White Leghorn chickens (Gallus gallus) were randomly divided into five groups: a vehicle control and four mesterolone treatment groups (4, 8, 12, and 16 mg/kg). Mesterolone was administered orally every three days for 4 weeks. Immunocytochemical techniques and morphometric analyses were employed to measure the changes in muscle weight, fiber size, satellite cell (SC) composition, and number of myonuclei.

Results: Mesterolone increased both body and muscle weights and induced hypertrophy in glycolytic PM fibers but not in oxidative ALD fibers. Mesterolone induced SC proliferation in both muscles; however, the myonuclear accretion was noticeable only in the PM muscle. In both muscles, the collective changes maintained a constant myonuclear domain size and the changes were dose independent.

Conclusion: Mesterolone induced distinct dose-independent effects in avian oxidative and glycolytic skeletal muscle fibers; these findings might be clinically valuable in the treatment of age-related sarcopenia.

Funds for this study were provided by grants to M. Z. Allouh from Jordan University of Science amp;amp; Technology (Grants # 20150145 and 20150290) and from the United Arab Emirates University Al Ain, UAE (Grant # G00003289).