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Numerous corpora lutea form from the multiple follicles that ovulate during the oestrous cycle of pigs. Vascular elements invade the follicle from the theca compartment, first centripetally, and subsequently by lateral branching of centripetal veins and arteries. The vessels are the vehicle for dispersion of steroidogenic theca cells throughout the corpus luteum. Mitosis occurs in both the theca and granulosa layers before ovulation, and in luteal cells well into the luteal phase. Luteal cell proliferation undergoes gradual restriction as the corpus luteum matures, but the mechanisms of exit from the cell cycle are unknown. The extracellular ligands that direct luteinization and maintain the corpus luteum include LH, prolactin, insulin and insulin-like growth factors (IGFs). These ligands induce qualitative and quantitative changes in steroid output, with progesterone as the principal product. These changes upregulate the cholesterol synthetic pathways to increase substrate availability. The intracellular regulation of luteinization is complex. A model is presented in which LH stimulates arachidonic and lineoleic acid metabolism to produce ligands for the nuclear proteins of the peripheral peroxisome activator receptor family. These ligands have downstream effects on cell differentiation and exit from the cell cycle. Luteal function is maintained by interactions among ligands, cholesterol regulatory proteins and constitutively expressed and regulated transcription factors.

Formation and early development of the corpus luteum in pigs