Lipid droplets and metabolic pathways regulate steroidogenesis in the corpus luteum

This review focuses on recent advances in the understanding of metabolic processes used by the corpus luteum to control steroidogenesis and other cellular functions. The corpus luteum has abundant lipid droplets that are believed to store cholesteryl esters and triglycerides. Recent studies in other tissues indicate that cytoplasmic lipid droplets serve as platforms for cell signaling and interactions with other organelles. Lipid droplets are also critical organelles for controlling cellular metabolism. Emerging evidence demonstrates that LH via activation of the cAMP and the protein kinase A (PKA) signaling pathway stimulates the phosphorylation and activation of hormone-sensitive lipase (HSL), an enzyme that hydrolyzes cholesteryl esters stored in lipid droplets to provide cholesterol for steroidogenesis and fatty acids for utilization by mitochondria for energy production. The energy sensor AMP-activated protein kinase (AMPK) can inhibit steroidogenesis by interrupting metabolic pathways that provide cholesterol to the mitochondria or the expression of genes required for steroidogenesis. In addition to lipid droplets, autophagy also contributes to the regulation of the metabolic balance of the cell by eliminating damaged organelles and providing cells with essential nutrients during starvation. Autophagy in luteal cells is regulated by signaling pathways that impact AMPK activity and lipid droplet homeostasis. In summary, a number of signaling pathways converge on luteal lipid droplets to regulate steroidogenesis and metabolism. Knowledge of metabolic pathways in luteal cells is fundamental to understanding events that control the function and lifespan of the corpus luteum.