Abstract
Laboratory mouse models with genetically altered growth hormone (GH) signaling and subsequent endocrine disruptions, have longer lifespans than control littermates. As such, these mice are commonly examined to determine the role of the somatotropic axis as it relates to healthspan and longevity in mammals. The two most prominent mouse mutants in this context are the genetically dwarf Ames and Snell models which have been studied extensively for over two decades. However, it has only been proposed recently that both white and brown adipose tissue depots may contribute to their delayed aging. Here we review the current state of the field and supplement it with recent data from our labs.
Highlights
Aging and the Somatotropic Axis: A Focus on Ames and Snell MiceIt is well accepted in the biology of aging that insulin-like growth factor 1 (IGF-1) and insulin signaling relate to longevity in an evolutionarily conserved manner [1,2]
While Ames dwarf (AD) mice have been successfully maintained in a conventional laboratory environment [8,11,19], Snell dwarf (SD) mice have to be kept in filter-hooded cages in a specific pathogen-free environment and need chlorinated drinking water acidified to prevent the growth of Pseudomonas [35], all of which is increasingly becoming today’s standard maintenance conditions of laboratory rodents
We elaborated on specific husbandry requirements in genetically dwarf mice and initiated first evaluations of brown adipose tissue (BAT) function in SD mice
Summary
It is well accepted in the biology of aging that insulin-like growth factor 1 (IGF-1) and insulin signaling relate to longevity in an evolutionarily conserved manner [1,2]. While GH is secreted from the pituitary, IGF-1 as well as its auxiliary hormones, proteins, and receptors are synthesized in the liver and together these components form the pituitary-somatotropic axis [1,4,5,6] To this end, many mutations that affect the somatotropic axis have been extensively explored in mice to understand the functional relationships between GH, IGF-I, and lifespan (reviewed in [1,4,7]). InTable addition to stunted growth, AD is clearly recognizable even wellare before weaning. Inin addition to stunted growth, ADthroughout and and SD SD have a number ofwhich phenotypical similarities that summarized.
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