**Abstract**

Pituitary cell function is impacted by metabolic states and therefore must receive signals that inform them about nutritional status or adiposity. A primary signal from adipocytes is leptin, which recent studies have shown regulates most pituitary cell types. Subsets of all pituitary cell types express leptin receptors and leptin has been shown to exert transcriptional control through classical JAK/STAT pathways. Recent studies show that leptin also signals through post-transcriptional pathways that involve the translational regulatory protein Musashi. Mechanistically, posttranscriptional control would permit rapid cellular regulation of critical pre-existing pituitary transcripts as energy states change. The chapter will review evidence for transcriptional and/or post-transcriptional regulation of leptin targets (including *Gnrh*r, activin, *Fshb, Gh, Ghrhr,* and *Pou11f1*) and the consequences of the loss of leptin signaling to gonadotrope and somatotrope functions.

**Keywords:** Leptin, somatotropes, gonadotropes, Musashi, post-transcriptional, *Pou1f1*, *Ghrhr*, *Gnrhr*, *Fshb*
