**9. Conclusions**

Pituitary gonadotropes and somatotropes were initially shown to be most vulnerable to the global loss in leptin signals as demonstrated by their reduction in numbers in the population, even following acute fasting. As little as 10-100 pg./ml leptin directly restored hormone levels in these populations, so they could once more be detected by immunolabeling. We now have much more information about the impact of loss of leptin signaling to model animals including infertility when they carried LEPR-null gonadotropes and adult-onset obesity and GH deficiency when they carried LEPR-null somatotropes. We have identified specific leptin targets in each of these cell types and determined that leptin regulation may involve both transcriptional and post-transcriptional pathways. The target molecules are vital to the differentiated function of these cells, which highlights a role for leptin in maintaining their differentiated state. Regarding post-transcriptional pathways, we have shown that leptin also regulates expression of the translational regulatory protein, Musashi. Our studies have led to the discovery of novel roles for Musashi, implicating this regulator in the repression of targets in specific pituitary cell types. This broadens the scope of Musashi's regulatory role beyond that of regulation of stem cells. Finally, our studies of purified somatotropes and gonadotropes have confirmed the presence of multihormonal expression in a subpopulation of cells and have led to the discovery that leptin signaling is needed to maintain this subset. The presence of these multihormonal pituitary cells is also evident in single cell RNA-sequencing studies. Future studies are needed that focus on the role leptin plays in maintaining this cell population, which supports pituitary plasticity. Future investigation will elucidate the role Musashi may play in the selective regulation of specific hormones or their transcription factors.
