When ZPA cells, non-ZPA cells made to express shh, or simply shh protein-soaked beads are implanted in the anterior side of a limb bud, the end of the resulting limb is duplicated, as in diplopodia. The posterior autopod on that limb has the normal orientation, and the extra, anterior autopod has a reversed anterior-posterior axis. This is because the original ZPA and the added source of shh signaling each induce the formation of an autopod. Diplopodia in humans
Diplopodia is often found in combination with aplasia or hypoplasia of the tibia. Sometimes, the tibia is replaced by another fibula The extra foot is almost always joined to the normal foot, though a case was described where a nearly complete extra foot joined to the back of the ankle. Diplopodia in chickens
People have identified five recessive lethal mutations in chickens that cause bilateral diplopodia. The genes are numbered in the order of their discoveries, with the symbols dp-1, dp-2, dp-3, dp-4, and dp-5. Chickens normally have an anisodactyl toe arrangement, with one short toe pointing backwards and three long toes pointing forwards. In diplopodia, the feet usually lack the normal hind toe and instead develop two to four extra toes at various positions between the hock joint and the front toes. The toes are almost always connected to extra tarso-metatarsal bones, though sometimes the toes do not contain any bone. Embryos with diplopodia have been found with numbers of digits on one wing ranging from one to seven, while normal embryos have three digits per wing.
Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis, is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty. Signs of puberty can develop as early as an age of 1 year.The spinal length in boys may be short due to a rapid advance in epiphyseal maturation. It is an autosomal dominant condition with a mutation of the luteinizing hormone (LH) receptor. As FMPP is a gonadotropin-independent form of precocious puberty, gonadotropin-releasing hormone agonists (GnRH agonists) are ineffective. Treatment is with drugs that suppress or block the effects of gonadal steroidogenesis, such as cyproterone acetate, ketoconazole, spironolactone, and testolactone. Alternatively, the combination of the androgen receptor antagonist bicalutamide and the aromatase inhibitor anastrozole may be used.Robert King Stone, personal physician to American president Abraham Lincoln, described the first case of FMPP in 1852. See also
Follicle-stimulating hormone insensitivity
Gonadotropin-releasing hormone insensitivity
Hypergonadism, hyperandrogenism, and precocious puberty
Inborn errors of steroid metabolism
Leydig cell hypoplasia (or LH insensitivity)

References
External links
Testotoxicosis at NIHs Office of Rare Diseases