From a wide range of mammals, including humans (Ferraù and Korbonits, 2015), dogs (Kooistra and Galac, 2012), horses (McCue, 2002), cats (Meijer et al., 1978), and guinea pigs (Zeugswetter et al., 2007), it is known that chronic glucocorticoid excess leads to a number of pathological symptoms that largely overlap with those of aging and result in considerably higher mortality rates for affected individuals (Etxabe and Vazquez, 1994, #808). The most common cause of chronic glucocorticoid excess is excessive secretion of the adrenocorticotropic hormone (ACTH) by the pituitary gland. ACTH is transported via the blood to the adrenal cortex where it binds to the ACTH-receptor (ACTHR; encoded by the gene MC2R), which induces the production of glucocorticoids, especially cortisol. Glucocorticoids are transported to the various tissues, where they exert their effect by activating the glucocorticoid receptor (NR3C1) that acts as a transcription factor and regulates hundreds of genes. The constant overuse of this transcriptional pattern eventually leads to the listed symptoms. Our hypothesis is that the permanent, high expression of the ACTH-receptor in Fukomys non-breeders causes effects similar to those known from overproduction of the hormone. In line with this hypothesis, (i) cortisol levels are increased in non-breeders and (ii) target genes of the glucocorticoid receptor are highly enriched for status-dependent differential gene expression. Furthermore, the animals were examined for common symptoms of chronic glucocorticoid excess: (iii) non-breeders gained more weight during the experiment than breeders, (iv) exhibited lower bone density at the end of the experiment, and (v) lower gene expression in the growth hormone/insulin-like growth factor 1 axis than breeders.