Endocrine control of mammalian longevity was first reported in Ames dwarf (Prop1<sup>df</sup>) mice, which are long-lived due to a recessive Prop1 loss-of-function mutation resulting in deficiency of growth hormone (GH), thyroid-stimulating hormone, and prolactin.
In mammals, this is exemplified in Ames dwarf (Prop1<sup>df/df</sup>) mice, which have a 40%-60% increase in longevity (males and females, respectively) due to their recessive Prop1 loss-of-function mutation that results in lack of growth hormone (GH), thyroid-stimulating hormone and prolactin.
Mutations of the pituitary transcription factor gene POU1F1 (the human homologue of mouse Pit1) are responsible for deficiencies of GH, prolactin and thyroid stimulating hormone (TSH) in Snell and Jackson dwarf mice and in man, while the production of adrenocorticotrophic hormone (ACTH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) is preserved.
Animals and appropriate controls studied included 16-day pregnant, two lines of human GH-expressing transgenic, and two lines of pituitary PRL- and GH-deficient dwarf mice.