Abstract
The etiology of cystic ovarian follicles (COF) remains a conundrum with steroidogenic, immunological, and metabolic dysfunctions linked to its development. Studies suggest that COF development may occur as a result of disruption of the insulin signaling pathway and the severity of a negative energy balance in dairy cows, but mid to late lactation cows diagnosed with COF are unlikely to have issues with energy metabolism. Herein, we characterized the mRNA expression of steroidogenic (LHCGR, StAR, CYP11A1, 3β-HSD, CYP19A), immunological (IL-1β, IL-6, IL-8, TLR-4, TNF), and metabolic markers (IGF-1, IRS1) in follicular fluid; and plasma and follicular fluid levels of E2, IL-1β, glucose, and NEFA in early and mid-late lactation COF cows. Lactating dairy cows were diagnosed as having COF (n = 11, follicle >20 mm persistent for 7 days, absence of corpus luteum, and flaccid uterus) while 11 herdmates cycling with a dominant follicle were classified as the control cows. Cows diagnosed with COF were classified as early lactation (COF-E, n = 5) cows, <35 days in milk (DIM); or mid-late lactation (COF-M/L, n = 6), ≥118 DIM cows. Results revealed that mRNA expression StAR was greater (P < 0.01) in COF-E cows than COF-M/L cows and the control cows. The mRNA expression CYP19A1 was lower (P < 0.01) in COF-E cows and COF-M/L cows than in the control cows. The mRNA expression IL-6 and IRS-1 tended to be greater and lower, respectively, in COF-M/L cows compared to the control cows. The mRNA expression IGF-1 was greater (P < 0.01) in COF-E and COF-M/L cows than in the control cows. The plasma and follicular fluid concentration of NEFA was greater (P < 0.05) in COF-E cows than in COF-M/L and the control cows. Cows with COF-E had disturbances in steroidogenic and metabolic markers, while cows with COF-M/L had steroidogenic, immunological, and metabolic dysregulations, suggesting that COF pathogenesis may vary between early and mid-late lactation dairy cows.
Highlights
The etiology of cystic ovarian follicles (COF) remains a puzzle, but hormonal, immunological, and metabolic imbalances have been linked to its development [1,2,3,4,5]
Cow diagnosed with COF-E had a (P < 0.01) greater mRNA expression of steroid acute regulatory protein (StAR) than that of COF-M/L and the control cows (Figure 1B)
Cows diagnosed with COF-E and COF-M/L had a greater (P < 0.02) mRNA expression of insulin growth factor-1 (IGF-1) than the control herdmates (Figure 3A)
Summary
The etiology of cystic ovarian follicles (COF) remains a puzzle, but hormonal, immunological, and metabolic imbalances have been linked to its development [1,2,3,4,5]. Cows diagnosed with COF have a dysfunctional hypothalamic-pituitary-ovarian axis signature that includes parabasal concentration of progesterone, increased peripheral estradiol levels, increased LH pulse frequency and amplitude, and reduced LH and FSH receptors that translate into a lack of LH surge and ovulation [6,7,8,9,10]. The steroidogenic markers associated with this dysfunctional signature is not well elucidated. A more recent study found a higher or lower protein expression steroid acute regulatory protein (StAR), cytochrome P450 aromatase (CYP19A1), and 3β-hydroxysteroid dehydrogenase (3β-HSD) in the theca and granulosa cells of COF depending on the follicular stage of development [5]. The characterization of steroidogenic markers between early and mid-late lactation cows developing COF might help to improve the understanding the differences in COF pathogenesis
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