Asprosin is a novel fasting-induced protein associated with insulin resistance and polycystic ovaries in humans. It is encoded by FBN1 gene and produced when FBN1 is cleaved by the enzyme furin. In cattle, the role of asprosin is unknown. To characterize mRNA abundance of FBN1, furin, and the asprosin receptor, OR4M1, in granulosa (GC) and theca cells (TC), and identify hormones regulating FBN1 mRNA expression, GC and TC from small (< 6 mm; SM) and large (>5 mm; LG) follicles were collected from heifers at an abattoir and used for real-time gene expression analysis or in vitro evaluation of hormone regulation. SMTC had 151-fold greater (P < 0.05) FBN1 mRNA abundance than SMGC, and LGTC had 50-fold greater (P < 0.05) FBN1 mRNA than LGGC. In contrast, OR4M1 mRNA abundance was significantly greater (by 81-fold) in SMGC than LGGC and did not differ from SMTC, but LGTC had 9-fold greater (P < 0.05) OR4M1 mRNA abundance than LGGC. Furin mRNA was significantly greater (by 2.6-fold) in SMGC than SMTC but did not differ between LGTC and LGGC. In SMGC, leptin, insulin, GH, FSH, EGF, and steroids had no effect (P >0.10) on FBN1 mRNA abundance. In contrast, TGFB1, WNT3A and FGF9 increased (P < 0.05) and IGF1 significantly decreased SMGC FBN1 mRNA abundance. In LGTC, leptin, insulin, LH, IGF1 and steroids did not significantly affect FBN1 mRNA, but TGFB1, WNT3A, EGF, FGF2 and FGF9 increased (P< 0.05) FBN1 mRNA abundance. Altogether, FBN1 mRNA was more highly expressed in TC than GC and was stimulated by TGFB1, WNT3A and FGF9 in both cell types. Developmental and hormonal regulation of FBN1, furin and OR4M1 along with a greater expression of OR4M1 mRNA in GC than TC suggests that asprosin may be acting as a paracrine regulator of ovarian follicular function in cattle.

ER Maylem, L Spicer, I Batalha, L Schutz 2020, Developmental and hormonal regulation of gene expression of fibrillin-1 (FBN1) and the asprosin receptor, olfactory receptor family 4 subfamily M member 1 (OR4M1), in bovine ovarian cells, Journal of Animal Science, Volume 98, Issue Supplement 4

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