Effects of Dietary Exemestane Administration on Reproductive Performance, Hepatic Function, and Lipid Metabolism in Japanese Quail

Estrogen is a central regulator of avian reproduction and metabolism, with key functions in vitellogenesis and hepatic lipid mobilization. This study evaluated the physiological effects of dietary exemestane administration, using a compound pharmacologically classified as an irreversible steroidal aromatase inhibitor, on reproductive performance, serum lipid indices, hepatic enzyme activity, egg quality, yolk lipid peroxidation, and yolk fatty acid composition in Japanese quail (Coturnix japonica). A total of 192 28-day-old female quail were acclimated for 14 days on a basal diet and subsequently fed experimental diets containing 0 (control), 0.5, 1.0, or 1.5 mg/kg exemestane from 43 days of age for 56 days. Reproductive performance traits were recorded throughout the trial, whereas serum biochemical variables, hepatic enzyme activities, egg-quality traits, and yolk oxidative and fatty acid indices were evaluated at the end of the experimental period. Dietary exemestane did not significantly affect overall egg production or egg weight. However, birds receiving 1.5 mg/kg exemestane exhibited reduced eggshell percentage, altered serum HDL cholesterol, increased aspartate aminotransferase activity, and markedly higher yolk lipid peroxidation, suggesting dose-related metabolic and oxidative responses at the highest inclusion level. Exemestane administration also produced selective alterations in yolk fatty acid composition, including changes in monounsaturated and n-3 fatty acid fractions. Overall, these findings indicate that dietary exemestane administration is associated with dose-dependent changes in metabolic and egg-quality traits without marked impairment of reproductive output. Because circulating sex steroids, gonadotropins, tissue CYP19A expression, and aromatase activity were not directly measured, these results should be interpreted as physiological responses compatible with estrogen-sensitive pathway modulation rather than as direct empirical confirmation of aromatase inhibition.