Unraveling the mechanisms of ovulatory failure in dairy cows: The role of lipid metabolism

Abstract

Ovulatory failure in dairy cows can stem from various causes, including the formation of follicular cysts, which disrupt the estrous cycles and extend reproductive intervals, ultimately hindering herd management and reproductive performance. Reproductive dysfunctions are frequently associated with metabolic disorders, commonly observed in these animals. Therefore, this study aimed to evaluate key components of lipid metabolism, primarily related to β-oxidation, including AdipoR1, AdipoR2, AMPK, PPARγ, ObR, ACC1, CPT1, and ACOX1 in ovary, as well as adiponectin, leptin, triglyceride (TG) and non-esterified fatty acid (NEFA) concentrations in plasma and follicular fluid of dairy cows with induced persistent follicles, spontaneous follicular cysts and dominant control follicles. Ovary protein immunoexpression was assessed in situ by immunohistochemistry, plasma and follicular fluid adiponectin and leptin concentrations were quantified by ELISA, and TG and NEFA concentrations were determined by colorimetric methods. The results indicated increased protein expression of adiponectin receptors in follicles of 15 days of persistence, along with an upregulation of CPT1 expression. ACC1 expression was lower in both follicles of 15 days of persistence and in spontaneous cysts than in preovulatory follicles. Furthermore, PPARγ expression was decreased in follicles of 15 days of persistence compared to dominant control follicles. These findings indicate changes in key molecules involved in ovarian lipid metabolism, with a pronounced shift towards β-oxidation pathways and decreased lipid synthesis and lipid storage. Such metabolic disruptions may contribute to impaired ovarian function, potentially leading to ovulatory failure of the preovulatory follicle.