The pro-opiomelanocortin (POMC) gene is expressed in the hypothalamus and pituitary and its product is cleaved into several peptides including the melanocyte stimulating hormones (α, β, or γ-MSH), adrenocorticotropic hormone (ACTH), and beta-endorphin. Alpha-MSH is involved in regulating appetite, sexual behavior, and melanin, while ACTH regulates secretion of glucocorticoids from the adrenal cortex. Humans who have a POMC mutation either produce an abnormally short version of POMC or are missing the protein completely and therefore lack these hormones. This has biological consequences including red hair and fair skin, early-onset obesity (due to severe hyperphagia), hypothyroidism, hypogonadism, and potentially infertility. We are interested in studying the infertility through a mouse model of hypothalamic POMC-deficiency. These mice also experience early-onset obesity and infertility. The testes and epididymides of these mice have been sliced and stained with hematoxylin and eosin, and then fixed to a slide. These slides will be placed under a microscope and imaged at 4x, 10x and 40x to determine the amount and condition of germ cells, somatic cells, and sperm. Some potential issues that could be identified through histology are tubular degeneration or atrophy, which causes shrinkage of the testis and loss of germ cells due to reduced testosterone and sperm levels. There may also be a disrupted blood-testes barrier due to obesity, which decreases the motility of the sperm. The results from this study will help us understand the causes of infertility in POMC-deficient mice, which may also lead to greater understanding on how to treat humans with infertility due to a POMC mutation.