No abstract

Each follicle represents the basic functional unit of the ovary. From its very initial stage of development, the follicle consists of an oocyte surrounded by somatic cells. The oocyte grows and matures to become fertilizable and the somatic cells proliferate and differentiate into the major suppliers of steroid sex hormones as well as generators of other local regulators. The process by which a follicle forms, proceeds through several growing stages, develops to eventually release the mature oocyte, and turns into a corpus luteum (CL) is known as “folliculogenesis”. The task of this review is to define the different stages of folliculogenesis culminating at ovulation and CL formation, and to summarize the most recent information regarding the newly identified factors that regulate the specific stages of this highly intricated process. This information comprises of either novel regulators involved in ovarian biology, such as Ube2i, Phoenixin/GPR73, C1QTNF, and α-SNAP, or recently identified members of signaling pathways previously reported in this context, namely PKB/Akt, HIPPO, and Notch.

This study aimed to identify individual characteristics differing among high-efficiency (HEf; upper 20%, n = 31), low-efficiency (LEf; lower 20%, n = 31), and mid-efficiency (MEf, 60% n = 93) lactating cows. Primiparous (37) and multiparous (118) high-producing milking cows at 30 to 180 d in milk were fed individually a low-roughage diet [31.6% of dry matter (DM)] for 4 wk. Daily average DM intake, rate of eating, visit duration, meal size, and daily rumination time were higher in LEf compared with HEf cows. On the other hand, HEf cows exhibited higher digestibility of DM, crude protein, and neutral detergent fiber than the LEf cows. Daily eating time was similar in the HEf and LEf groups and higher than that of the MEf cows. Visit and meal frequency, average visit and meal duration, daily lying time, and pedometer activity were similar in the HEf, LEf, and MEf groups. The HEf cows produced 1.75% more milk, but similar energy-corrected milk compared with the LEf cows. Milk fat and protein content were lower by 1.8 and 3.8%, respectively, in the HEf cows than in the LEf group. Body weight (BW) and BW gain were similar in the 3 efficiency groups. Diurnal distribution of DM intake showed 6 distinct major meals, each composed of 1.1 to 1.6 visits. Higher intake peaks (greater meal size) were found in the LEf cows compared with the HEf group. Daily DM intake was highly correlated (affected) with energy-corrected milk production (r = 0.61), BW (r = 0.4), eating rate (r = 0.57), and visit size (r = 0.54). Energy balance showed that the lower efficiency of the LEf cows was attributed to their excess heat production and energy loss.

Objective Ghrelin is known to regulate appetite control and cellular metabolism. The Corticotropin-Releasing Factor (CRF) family is also known to regulate energy balance. In this study, we investigated the links between ghrelin and the CRF family in C2C12 cells, a mouse myoblast cell line. Design and methods C2C12 cells were treated with ghrelin in the presence or absence of CRF receptor antagonists and then subjected to different metabolic analyses. Results Ghrelin enhanced glucose uptake by C2C12 cells, induced GLUT4 translocation to the cell surface and decreased RBP4 expression. A CRF-R2 selective antagonist, anti-sauvagine-30, blocked ghrelin-induced glucose uptake, Ghrelin upregulated CRF-R2 but not CRF-R1 levels. Moreover, ghrelin-treated C2C12 cells displayed a cAMP and pERK activation in response to Ucn3, a CRF-R2 specific ligand, but not in response to CRF or stressin, CRF-R1 specific ligands. Ghrelin also induced UCP2 and UCP3 expression, which were blocked by anti-sauvagine-30. Ghrelin did not induce fatty acids uptake by C2C12 cells or ACC expression. Even though C2C12 cells clearly exhibited responses to ghrelin, the known ghrelin receptor, GHSR1a, was not detectable in C2C12 cells. Conclusion Our results suggest that, ghrelin plays a role in regulating muscle glucose and, raise the possibility that suppression of the CRF-R2 pathway might provide benefits in high ghrelin states.

The SULT1E1-encoded estrogen sulfotransferase (EST) catalyzes sulfation of estrogen, resulting in its inactivation. Reduced fertility observed in SULT1E1 knockout (KO) female mice has previously been attributed to the deleterious effect of chronic exposure to high levels of circulating estrogen on placental function. We herein suggest that, in addition to placental dysfunction, this phenotype demonstrates that an excess of estrogen impairs ovulation. The role of SULT1E1 in ovulation is suggested by the substantially low ovulatory response in hCG-treated SULT1E1 KO mice; a similar effect was observed when 17beta-estradiol was administered to wild-type (WT) females. The normal rate of ovulation in SULT1E1 KO females may be restored by PGE2. Along this line, ovaries of human Chorionic Gonadotropin (hCG)-treated SULT1E1 KO mice expressed low levels of cyclooxygenase-2 (COX-2) and its downstream TSG6; moreover, their ovaries contained a reduced number of expanded cumuli. Our results demonstrate, for the first time, that estrogen inactivation may allow the expression of COX-2 and subsequent cumulus expansion, enabling normal ovulation. Our findings may be applied to novel treatments of human ovulatory failure.